How long is a tooth sensitive after a crown?


If you notice pain or sensitivity when you bite down after getting a crown, you should contact your dentist. Usually this MORE?

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A healthy tooth has a space inside it called the "pulp space" which is filled with soft tissues - nerves, blood vessels and pink connective tissue. If a tooth gets a large cavity, the bacteria in the decay can damage the pulp, which is often what causes toothache. Tooth-01.png Damage to the pulp of permanent teeth usually requires a Root Canal Treatment or Endodontic Therapy. The pulp of primary or deciduous teeth, which only have to survive until an adult teeth come in, and because they have a better blood supply, can sometimes be saved. Primary (Baby) teeth in children have relatively large pulp spaces and a cavity does not have to get very large before it reaches the pulp chamber. Tooth-02.png When the soft tissue in the pulp chamber is infected (has bacteria in it) or affected (is inflamed), it can be removed by a dentist under local anaesthetic. If the soft tissue in the canals is still healthy enough, a special medicated filling can be put into the chamber in an attempt to keep the remaining pulp (in the canals) alive. The process of removing the pulp from the chamber is the actual "pulpotomy", though the word is often used for the entire process including placement of the medication. Tooth-03.png Afterwards the tooth is restored with a regular filling or a stainless steel crown. Pulpotomies are only done in permanent teeth (adult teeth) as a temporary alternative to proper root canal therapy. For example, if there isn't enough time, the patient is traveling or they can't afford to have more conventional treatment. In some cases an adult tooth might have decay down to the pulp but the pulp is still pretty healthy. If the roots haven't finished forming yet, a partial pulpotomy might give it a chance to finish forming. A partial pulpotomy for traumatic exposures is also called a Cvek Pulpotomy. When a baby tooth or young permanent tooth is traumatised - say, hitting your teeth on the handlebars of a bike - it can be broken in such a way that the pulp is exposed. Again, a partial pulpotomy may help it to finish developing and be saved. In primary teeth medicaments such as formocresol, Ferric sulphate, and Calcium hydroxide can be used in pulpotomy although the clinical and radiographic success rate of ferric sulphate is higher than the other materials. It is known as non chemical devitalization. Its mechanism of action is the cauterization of the pulp tissue. It carburizes heat denaturated pulp and bacterial contamination. This technique overcomes histological effect of electro surgery. It creates superficial zone of coagulation necrosis that remain compatible with underlying tissue& isolate pulp from vigorous effects of the sub-base. 1. Maintenance of radicular portion vitality. 2. Clinical and radiographic evaluation should show no complications such as, pain, swelling, internal resorption or abnormal canal calcification. 3. Neither breakdown of the supporting tissue, nor trauma to succedaneous teeth should be detected. M: TTH anat/devp/phys noco/cong/jaws/tumr, epon, injr dent, proc (endo, orth, pros)
Tooth enamel, along with dentin, cementum, and dental pulp is one of the four major tissues that make up the tooth in humans, many other animals, and some species of fish. It makes up the normally visible part of the tooth, covering the crown. It is the hardest substance in the human body and contains the highest percentage of minerals, 96%, with water and organic material composing the rest. The primary mineral is hydroxyapatite, which is a crystalline calcium phosphate. Enamel is formed on the tooth while the tooth is developing within the gum, before it erupts into the mouth. Once fully formed, it does not contain blood vessels or nerves and when damaged cannot be repaired by the body. The maintenance and repair of human tooth enamel is one of the primary concerns of dentistry. In humans, enamel varies in thickness over the surface of the tooth, often thickest at the cusp, up to 2.5 mm, and thinnest at its border with the cementum at the cementoenamel junction (CEJ). The normal color of enamel varies from light yellow to grayish (bluish) white. At the edges of teeth where there is no dentin underlying the enamel, the color sometimes has a slightly blue tone. Since enamel is semitranslucent, the color of dentin and any material underneath the enamel strongly affects the appearance of a tooth. The enamel on primary teeth has a more opaque crystalline form and thus appears whiter than on permanent teeth. The large amount of mineral in enamel accounts not only for its strength but also for its brittleness. Tooth enamel ranks 5 on Mohs hardness scale and has a Young's modulus of 83 GPa. Dentin, less mineralized and less brittle, 3–4 in hardness, compensates for enamel and is necessary as a support. On radiographs, the differences in the mineralization of different portions of the tooth and surrounding periodontium can be noted; enamel appears lighter than dentin or pulp since it is denser than both and more radiopaque. Enamel does not contain collagen, as found in other hard tissues such as dentin and bone, but it does contain two unique classes of proteins - amelogenins and enamelins. While the role of these proteins is not fully understood, it is believed that they aid in the development of enamel by serving as a framework for minerals to form on, among other functions. Once it is mature, enamel is almost totally absent of the softer organic matter. Enamel is avascular and has no nerve supply within it and is not renewed, however, it is not a static tissue as it can undergo mineralization changes. The basic unit of enamel is called an enamel rod. Measuring 4–8 μm in diameter, an enamel rod, formally called an enamel prism, is a tightly packed mass of hydroxyapatite crystals in an organized pattern. In cross section, it is best compared to a keyhole, with the top, or head, oriented toward the crown of the tooth, and the bottom, or tail, oriented toward the root of the tooth. The arrangement of the crystals within each enamel rod is highly complex. Both ameloblasts (the cells which initiate enamel formation) and Tomes' processes affect the crystals' pattern. Enamel crystals in the head of the enamel rod are oriented parallel to the long axis of the rod. When found in the tail of the enamel rod, the crystals' orientation diverges slightly(65 degrees) from the long axis. The arrangement of enamel rods is understood more clearly than their internal structure. Enamel rods are found in rows along the tooth, and within each row, the long axis of the enamel rod is generally perpendicular to the underlying dentin. In permanent teeth, the enamel rods near the cementoenamel junction (CEJ) tilt slightly toward the root of the tooth. Understanding enamel orientation is very important in restorative dentistry, because enamel unsupported by underlying dentin is prone to fracture. The area around the enamel rod is known as interrod enamel. Interrod enamel has the same composition as enamel rod, however a histologic distinction is made between the two because crystal orientation is different in each. The border where the crystals of enamel rods and crystals of interrod enamel meet is called the rod sheath. Striae of Retzius are incremental lines that appear brown in a stained section of mature enamel. These lines are composed of bands or cross striations on the enamel rods that, when combined in longitudinal sections, seem to traverse the enamel rods. Formed from changes in diameter of Tomes’ processes, these incremental lines demonstrate the growth of enamel, similar to the annual rings on a tree on transverse sections of enamel. The exact mechanism that produces these lines is still being debated. Some researchers hypothesize that the lines are a result of the diurnal, or 24 hour, metabolic rhythm of the ameloblasts producing the enamel matrix, which consists of an active secretory work period followed by an inactive rest period during tooth development. Thus, each band on the enamel rod demonstrates the work/rest pattern of the ameloblasts that generally occurs over a span of a week. Perikymata which are associated with the Striae are shallow grooves noted clinically on the nonmasticatory surfaces of some teeth in the oral cavity. Perikymata are usually lost through tooth wear, except on the protected cervical regions of some teeth, especially the permanent maxillary central incisors, canines, and first premolars, and may be confused as dental calculus. Darker than the other incremental lines, the neonatal line is an incremental line that separates enamel formed before and after birth. The neonatal line marks the stress or trauma experienced by the ameloblasts during birth, again illustrating the sensitivity of the ameloblasts as they form enamel matrix. As one would expect, the neonatal line is found in all primary teeth and in the larger cusps of the permanent first molars. They contain irregular structures of enamel prisms with disordered crystal arrangements basically formed by the abrupt bending of the prisms towards the root; usually, the prisms gradually bent back again to regain their previous orientation. Gnarled enamel is found at the cusps of teeth. Its twisted appearance results from the orientation of enamel rods and the rows in which they lie.
Enamel formation is part of the overall process of tooth development. When the tissues of the developing tooth are seen under a microscope, different cellular aggregations can be identified, including structures known as the enamel organ, dental lamina, and dental papilla. The generally recognized stages of tooth development are the bud stage, cap stage, bell stage, and crown, or calcification, stage. Enamel formation is first seen in the crown stage. Amelogenesis, or enamel formation, occurs after the first establishment of dentin, via cells known as ameloblasts. Human enamel forms at a rate of around 4 μm per day, beginning at the future location of cusps, around the third or fourth month of pregnancy. As in all human processes, the creation of enamel is complex, but can generally be divided into two stages. The first stage, called the secretory stage, involves proteins and an organic matrix forming a partially mineralized enamel. The second stage, called the maturation stage, completes enamel mineralization. In the secretory stage, ameloblasts are polarized columnar cells. In the rough endoplasmic reticulum of these cells, enamel proteins are released into the surrounding area and contribute to what is known as the enamel matrix, which is then partially mineralized by the enzyme alkaline phosphatase. When this first layer is formed, the ameloblasts move away from the dentin, allowing for the development of Tomes’ processes at the apical pole of the cell. Enamel formation continues around the adjoining ameloblasts, resulting in a walled area, or pit, that houses a Tomes’ process, and also around the end of each Tomes’ process, resulting in a deposition of enamel matrix inside of each pit. The matrix within the pit will eventually become an enamel rod, and the walls will eventually become interrod enamel. The only distinguishing factor between the two is the orientation of the calcium phosphate crystals. In the maturation stage, the ameloblasts transport substances used in the formation of enamel. Histologically, the most notable aspect of this phase is that these cells become striated, or have a ruffled border. These signs demonstrate that the ameloblasts have changed their function from production, as in the secretory stage, to transportation. Proteins used for the final mineralization process compose most of the transported material. The noteworthy proteins involved are amelogenins, ameloblastins, enamelins, and tuftelins. During this process, amelogenins and ameloblastins are removed after use, leaving enamelins and tuftelin in the enamel. By the end of this stage, the enamel has completed its mineralization. At some point before the tooth erupts into the mouth, but after the maturation stage, the ameloblasts are broken down. Consequently, enamel, unlike many other tissues of the body, has no way to regenerate itself. After destruction of enamel from decay or injury, neither the body nor a dentist can restore the enamel tissue. Enamel can be affected further by non-pathologic processes. Enamel is covered by various structures in relation to the development of tooth: Progress of enamel formation for primary teeth The high mineral content of enamel, which makes this tissue the hardest in the human body, also makes it susceptible to a demineralization process which often occurs as dental caries, otherwise known as cavities. Demineralization occurs for several reasons, but the most important cause of tooth decay is the ingestion of fermentable carbohydrates.][ Tooth cavities are caused when acids dissolve tooth enamel: Sugars from candies, soft drinks, and even fruit juices play a significant role in tooth decay, and consequently in enamel destruction. The mouth contains a great number and variety of bacteria, and when sucrose, the most common of sugars, coats the surface of the mouth, some intraoral bacteria interact with it and form lactic acid, which decreases the pH in the mouth. Then, the hydroxylapatite crystals of enamel demineralize, allowing for greater bacterial invasion deeper into the tooth. The most important bacterium involved with tooth decay is Streptococcus mutans, but the number and type of bacteria varies with the progress of tooth destruction. Furthermore, tooth morphology dictates that the most common site for the initiation of dental caries is in the deep grooves, pits, and fissures of enamel. This is expected because these locations are impossible to reach with a toothbrush and allow for bacteria to reside there. When demineralization of enamel occurs, a dentist can use a sharp instrument, such as a dental explorer, and "feel a stick" at the location of the decay. As enamel continues to become less mineralized and is unable to prevent the encroachment of bacteria, the underlying dentin becomes affected as well. When dentin, which normally supports enamel, is destroyed by a physiologic condition or by decay, enamel is unable to compensate for its brittleness and breaks away from the tooth easily. The extent to which tooth decay is likely, known as cariogenicity, depends on factors such as how long the sugar remains in the mouth. Contrary to common belief, it is not the amount of sugar ingested but the frequency of sugar ingestion that is the most important factor in the causation of tooth decay. When the pH in the mouth initially decreases from the ingestion of sugars, the enamel is demineralized and left vulnerable for about 30 minutes. Eating a greater quantity of sugar in one sitting does not increase the time of demineralization. Similarly, eating a lesser quantity of sugar in one sitting does not decrease the time of demineralization. Thus, eating a great quantity of sugar at one time in the day is less detrimental than is a very small quantity ingested in many intervals throughout the day. For example, in terms of oral health, it is better to eat a single dessert at dinner time than to snack on a bag of candy throughout the day. In addition to bacterial invasion, enamel is also susceptible to other destructive forces. Bruxism, also known as clenching of or grinding on teeth, destroys enamel very quickly. The wear rate of enamel, called attrition, is 8 micrometers a year from normal factors. A common misconception is that enamel wears away mostly from chewing, but actually teeth rarely touch during chewing. Furthermore, normal tooth contact is compensated physiologically by the periodontal ligaments (pdl) and the arrangement of dental occlusion. The truly destructive forces are the parafunctional movements, as found in bruxism, which can cause irreversible damage to the enamel. Other nonbacterial processes of enamel destruction include abrasion (involving foreign elements, such as toothbrushes), erosion (involving chemical processes, such as dissolving by soft drinks or lemon and other juices), and possibly abfraction (involving compressive and tensile forces). Though enamel is described as tough, it has a similar brittleness to glass making it, unlike other natural crack-resistant laminate structures such as shell and nacre, potentially vulnerable to fracture. In spite of this it can withstand bite forces as high as 1,000 N many times a day during chewing. This resistance is due in part to the microstructure of enamel which contains processes, enamel tufts, that stabilize the growth of such fractures at the dentinoenamel junction. The configuration of the tooth also acts to reduce the tensile stresses that cause fractures during biting. Gastroesophageal reflux disease can also lead to enamel loss, as acid refluxes up the esophagus and into the mouth, occurring most during overnight sleep. Considering the vulnerability of enamel to demineralization and the daily menace of sugar ingestion, prevention of tooth decay is the best way to maintain the health of teeth. Most countries have wide use of toothbrushes, which can reduce the number of dental biofilm and food particles on enamel. Some isolated societies do not have access to toothbrushes, but it is common for those people to use other objects, such as sticks, to clean their teeth. In between two adjacent teeth, floss is used to wipe the enamel surfaces free of plaque and food particles to discourage bacterial growth. Although neither floss nor toothbrushes can penetrate the deep grooves and pits of enamel, good general oral health habits can usually prevent enough bacterial growth to keep tooth decay from starting. Despite fluoridation's detractors, most dental professionals and organizations agree that the inclusion of fluoride in public water has been one of the most effective methods of decreasing the prevalence of tooth decay. Fluoride can be found in many locations naturally, such as the ocean and other water sources. The recommended dosage of fluoride in drinking water depends on air temperature. Fluoride catalyzes the diffusion of calcium and phosphate into the tooth surface, which in turn remineralizes the crystalline structures in a dental cavity. The remineralized tooth surfaces contain fluoridated hydroxyapatite and fluorapatite, which resist acid attack much better than the original tooth did . Fluoride therapy is used to help prevent dental decay. Fluoride ion, as an anitmicrobial, may activate bacteria fluoride-induced genes associated with fluoride riboswitches. The combination of fluoride ion and QAS was found stronger antimicrobial effect on many oral bacteria associated with dental decay, including S. mutans. Many groups of people have spoken out against fluoridated drinking water, for reasons such as the neurotoxicity of fluoride or the damage fluoride can do as fluorosis. Fluorosis is a condition resulting from the overexposure to fluoride, especially between the ages of 6 months to 5 years, and appears as mottled enamel. Consequently the teeth look unsightly, although the incidence of dental decay in those teeth is very small. It is important, however, to note that all substances, even beneficial ones, are detrimental when taken in extreme doses. Where fluoride is found naturally in high concentrations, filters are often used to decrease the amount of fluoride in water. For this reason, codes have been developed by dental professionals to limit the amount of fluoride a person should take. These codes are supported by the American Dental Association and the American Academy of Pediatric Dentistry; Furthermore, whereas topical fluoride, found in toothpaste and mouthwashes, does not cause fluorosis, its effects are now considered more important than those of systemic fluoride, such as when drinking fluorinated water. However, systemic fluoride works topically as well with fluoride levels in saliva increase also when drinking fluoridated water. Lately, dental professionals are looking for other ways to present fluoride (such as in varnish) or other mineralizing products such Amorphous calcium phosphate to the community in the form of topical procedures. Mineralization of the incipient lesion instead of restoration later is a prime goal of most dental professionals. UK scientists at Bristol University and the University of Leeds Dental Institute have developed gels which can regenerate decayed or damaged tooth enamel. A peptide hydrogel is applied to the tooth. This forms into a protein scaffold onto which new enamel-forming calcium is deposited from the saliva. The scientists claim to have seen "highly significant" levels of repair in which signs of decay have been reversed months after a single application of the compound. Most dental restorations involve the removal of enamel. Frequently, the purpose of removal is to gain access to the underlying decay in the dentin or inflammation in the pulp. This is typically the case in amalgam restorations and endodontic treatment. Nonetheless, enamel can sometimes be removed before there is any decay present. The most popular example is the dental sealant. The process of placing dental sealants in the past involved removing enamel in the deep fissures and grooves of a tooth and replacing it with a restorative material. Presently, it is more common to only remove decayed enamel if present. In spite of this, there are still cases where deep fissures and grooves in enamel are removed in order to prevent decay, and a sealant may or may not be placed depending on the situation. Sealants are unique in that they are preventative restorations for protection from future decay and have shown to reduce the risk of decay by 55% over 7 years. Aesthetics is another reason for the removal of enamel. Removing enamel is necessary when placing crowns and veneers to enhance the appearance of teeth. In both of these instances, When unsupported by underlying dentin, that portion of the enamel is more vulnerable to fracture. Invented in 1955, acid-etching employs dental etchants and is used frequently when bonding dental restoration to teeth. This is important for long-term use of some materials, such as composites and sealants. By dissolving minerals in enamel, etchants remove the outer 10 micrometers on the enamel surface and make a porous layer 5–50 micrometers deep. This roughens the enamel microscopically and results in a greater surface area on which to bond. The effects of acid-etching on enamel can vary. Important variables are the amount of time the etchant is applied, the type of etchant used, and the current condition of the enamel. There are three types of patterns formed by acid-etching. Type 1 is a pattern where predominantly the enamel rods are dissolved; type 2 is a pattern where predominantly the area around the enamel rods are dissolved; and type 3 is a pattern where there is no evidence left of any enamel rods. Besides concluding that type 1 is the most favorable pattern and type 3 the least, the explanation for these different patterns is not known for certain but is most commonly attributed to different crystal orientation in the enamel. The discoloration of teeth over time can result from exposure to substances such as tobacco, coffee, and tea. The staining occurs in the interprismatic region internally on the enamel, which causes the tooth to appear darker or more yellow overall. In a perfect state, enamel is colorless, but it does reflect underlying tooth structure with its stains since light reflection properties of the tooth are low. Tooth whitening or tooth bleaching procedures attempt to lighten a tooth's color in either of two ways: by chemical or mechanical action. Working chemically, a bleaching agent is used to carry out an oxidation reaction in the enamel and dentin. The agents most commonly used to intrinsically change the color of teeth are hydrogen peroxide and carbamide peroxide. Oxygen radicals from the peroxide in the whitening agents contact the stains in the interprismatic spaces within the enamel layer. When this occurs, stains will be bleached and the teeth now appear lighter in color. Teeth not only appear whiter but also reflect light in increased amounts, which makes the teeth appear brighter as well. Studies show that whitening does not produce any ultrastructural or microhardness changes in the dental tissues. Studies show that patients who have whitened their teeth take better care of them. However, a tooth whitening product with an overall low pH can put enamel at risk for decay or destruction by demineralization. Consequently, care should be taken and risk evaluated when choosing a product which is very acidic. Tooth whiteners in toothpastes work through a mechanical action. They have mild abrasives which aid in the removal of stains on enamel. Although this can be an effective method, it does not alter the intrinsic color of teeth. Microabrasion techniques employ both methods. An acid is used first to weaken the outer 22–27 micrometers of enamel in order to weaken it enough for the subsequent abrasive force. This allows for removal of superficial stains in the enamel. If the discoloration is deeper or in the dentin, this method of tooth whitening will not be successful. There are different types of amelogenesis imperfecta. The hypocalcification type, which is the most common, is an autosomal dominant condition that results in enamel that is not completely mineralized. Consequently, enamel easily flakes off the teeth, which appear yellow because of the revealed dentin. The hypoplastic type is X-linked and results in normal enamel that appears in too little quantity, having the same effect as the most common type. Chronic bilirubin encephalopathy, which can result from erythroblastosis fetalis, is a disease which has numerous effects on an infant, but it can also cause enamel hypoplasia and green staining of enamel. Enamel hypoplasia is broadly defined to encompass all deviations from normal enamel in its various degrees of absence. The missing enamel could be localized, forming a small pit, or it could be completely absent. Erythropoietic porphyria is a genetic disease resulting in the deposition of porphyrins throughout the body. These deposits also occur in enamel and leave an appearance described as red in color and fluorescent. Fluorosis leads to mottled enamel and occurs from overexposure to fluoride. Tetracycline staining leads to brown bands on the areas of developing enamel. Children up to age 8 can develop mottled enamel from taking tetracycline. As a result, tetracycline is contraindicated in pregnant women. Celiac disease, a disorder characterized by an auto-immune response to gluten, also commonly results in demineralization of the enamel. For the most part, research has shown that the formation of tooth enamel in animals is almost identical to formation in humans. The enamel organ, including the dental papilla, and ameloblasts function similarly. The variations of enamel that are present are infrequent but sometimes important. Differences exist, certainly, in the morphology, number, and types of teeth among animals. Dogs are less likely than humans to have tooth decay due to the high pH of dog saliva, which prevents an acidic environment from forming and the subsequent demineralization of enamel which would occur. In the event that tooth decay does occur (usually from trauma), dogs can receive dental fillings just as humans do. Similar to human teeth, the enamel of dogs is vulnerable to tetracycline staining. Consequently, this risk must be accounted for when tetracycline antibiotic therapy is administered to young dogs. Enamel hypoplasia may also occur in dogs. The mineral distribution in rodent enamel is different from that of monkeys, dogs, pigs, and humans. In horse teeth, the enamel and dentin layers are intertwined with each other, which increases the strength and wear resistance of those teeth. Tooth enamel is found in the dermal denticles of sharks. Enamel-like substances also coat the jaws of some crustacea. Enameloid covers some fish scales. Incisor: Central incisor, Lateral incisor, Canine Premolar: First premolar, Second premolar Incisor Central incisor, Lateral incisor, Canine Premolar: First premolar, Second premolar Crown: Cusp (Cusp of Carabelli) Pulp  Root canal (Apical foramen) Cementoenamel junction  Enamel  Dental-enamel junction  Dentin  Dental papilla Mammelon M: TTH anat/devp/phys noco/cong/jaws/tumr, epon, injr dent, proc (endo, orth, pros)
Temporomandibular joint dysfunction (sometimes abbreviated to TMD or TMJD and also termed temporomandibular joint dysfunction syndrome, temporomandibular disorder or many other names), is an umbrella term covering pain and dysfunction of the muscles of mastication (the muscles that move the jaw) and the temporomandibular joints (the joints which connect the mandible to the skull). The most important feature is pain, followed by restricted mandibular movement, and noises from the temporomandibular joints (TMJ) during jaw movement. Although TMD is not life threatening, it can detriment quality of life, because the symptoms can become chronic and difficult to manage. TMD is thought to be very common. About 20-30% of the adult population are affected to some degree. Usually people affected by TMD are between 20 and 40 years of age, and it is more common in females than males. TMD is the second most frequent cause of orofacial pain after dental pain (e.g. toothache). TMD is a symptom complex rather than a single condition, and it is thought to be caused by multiple factors. However, these factors are poorly understood, and there is disagreement as to the relative importance of these factors with each other. There are many treatments available, although there is a general lack of evidence for any treatment in TMD, and no widely accepted treatment protocol exists. Common treatments that are used include provision of occlusal splints, psychosocial interventions like cognitive behavioural therapy, and medications like analgesics (pain killers) or others. Most sources now agree that no irreversible treatment should be carried out for TMD. TMD is considered by some to be one of the 4 major symptom complexes in chronic orofacial pain, along with burning mouth syndrome, atypical facial pain and atypical odontalgia. TMD has been considered as a type of musculoskeletal, neuromuscular, or rheumatological disorder. It has also been called a functional pain syndrome, and a psychogenic disorder. Others consider TMD a "central sensitivity syndrome", in reference to evidence that TMD might be caused by a centrally mediated sensitivity to pain. It is hypothesized that there is a great deal of similarity between TMD and other pain syndromes like fibromyalgia, irritable bowel syndrome, interstitial cystitis, headache, chronic lower back pain and chronic neck pain. These disorders have also been theorized to be caused by centrally mediated sensitivity to pain, and furthermore they often occur together. Frequently, TMD has been treated as a single syndrome, but the prevailing modern view is that TMD is a cluster of related disorders with many common features. Indeed, some have suggested that in the future the term TMD may be discarded as the different causes are fully identified and separated into different conditions. Sometimes, "temporomandibular joint dysfunction" is described as the most common form of temporomandibular disorder, whereas many other sources use the term temporomandibular disorder synonymously, or instead of the term temporomandibular joint dysfunction. In turn, the term temporomandibular disorder is described as "a clinical term [referring to] musculoskeletal disorders affecting the temporomandibular joints and their associated musculature. It is a collective term which represents a diverse group of pathologies involving the temporomandibular joint, the muscles of mastication, or both". Another definition of temporomandibular disorders is "a group of conditions with similar signs and symptoms that affect the termporomandibular joints, the muscles of mastication, or both." Temporomandibular disorder is a term that creates confusion since it refers to a group of similarly symptomatic conditions, whilst many sources use the term temporomandibular disorders as a vague description rather than a specific syndrome, and refer to any condition which may affect the temporomandibular joints (see table). The temporomandibular joint is susceptible to a huge range of diseases, some rarer than others, and there is no implication that all of these will cause any symptoms or limitation in function at all. The preferred terms in medical publications is to an extent influenced by geographic location, e.g. in the United Kingdom, the term "pain dysfunction syndrome" is in common use, and in other countries different terms are used. In the United States, the term "temporomandibular disorder" is generally favored. The American Academy of Orofacial Pain uses temporomandibular disorder, whilst the National Institute of Dental and Craniofacial Research uses temporomandibular joint disorder. It is common for sources to arbitrarily use a preferred term and then list a handful of other synonyms. A more complete list of synonyms for this topic is extensive, with some being more commonly used than others. In addition to those already mentioned, examples include "temporomandibular joint pain dysfunction syndrome", "temporomandibular pain dysfunction syndrome", "temporomandibular joint syndrome", "temporomandibular dysfunction syndrome", "temporomandibular dysfunction", "temporomandibular disorder", "temporomandibular syndrome", "facial arthromyalgia", "myofacial pain dysfunction syndrome", "craniomandibular dysfunction", "myofacial pain dysfunction", "masticatory myalgia", "mandibular dysfunction", and "Costen's syndrome". The lack of standardization in terms is not restricted to medical papers. Notable internationally recognized sources vary in both their preferred term, and their offered definition, e.g. "Temporomandibular Pain and Dysfunction Syndrome - Aching in the muscles of mastication, sometimes with an occasional brief severe pain on chewing, often associated with restricted jaw movement and clicking or popping sounds." (Classification of Chronic Pain, International Association for the Study of Pain). "Headache or facial pain attributed to temporomandibular joint disorder." (International Classification of Headache Disorders 2nd edition (ICHD-2), International Headache Society). "Temporomandibular joint-pain-dysfunction syndrome" listed in turn under "Temporomandibular joint disorders" (International Classification of Diseases 10th revision, World Health Organization). In this article, the term temporomandibular disorder is taken to mean any disorder than affects the temporomandibular joint, and temporomandibular joint dysfunction (here also abbreviated to TMD) is taken to mean symptomatic (e.g. pain, limitation of movement, clicking) dysfunction of the temporomandibular joint, however there is no single, globally accepted term or definition concerning this topic. It has been suggested that TMD may develop following trauma, particularly whiplash injury, although the evidence for this is not conclusive. This type of TMD is sometimes termed "posttraumatic TMD" (pTMD) to distinguish it from TMD of unknown cause, sometimes termed "idiopathic TMD" (iTMD). Sometimes muscle-related (myogenous) TMD (also termed myogenous TMD, or TMD secondary to myofascial pain and dysfunction) is distinguished from joint-related TMD (also termed arthogenous TMD, or TMD secondary to true articular disease), based upon whether the muscles of mastication or the TMJs themselves are predominantly involved. This classification, which effectively divides TMD into 2 syndromes, is followed by the American Academy of Orofacial Pain. However, since most people with TMD could be placed into both of these groups, which makes a single diagnosis difficult when this classification is used. The Research Diagnostic Criteria (RDC/TMD) allows for multiple diagnoses in an attempt to overcome the problems with other classifications. RDC/TMD considers temporomandibular disorders in 2 axes; axis I is the physical aspects, and axis II involves assessment of psychological status, mandibular function and TMD-related psychosocial disability. Axis I is further divided into 3 general groups. Group I are muscle disorders, group II are disc displacements and group III are joint disorders, although it is common for people with TMD to fit into more than one of these groups. Sometimes distinction is made between acute TMD, where symptoms last for less than 3 months, and chronic TMD, where symptoms last for more than 3 months. Not much is known about acute TMD since these individuals do not typically attend in secondary care (hospital). Signs and symptoms of temporomandibular joint disorder vary in their presentation and can be very complex, but are often simple. The symptoms will usually involve more than one of the various components of the masticatory system, muscles, nerves, tendons, ligaments, bones, connective tissue, and/or the teeth. The three classically described, cardinal signs and symptoms of TMD are: Other signs and symptoms have also been described, although these are less common and less significant than the cardinal signs and symptoms listed above. Examples include: The temporomandibular joints are the dual articulation of the mandible with the skull. Each TMJ is classed as a "ginglymoarthrodial" joint since it is both a ginglymus (hinging joint) and an arthrodial (sliding) joint, and involves the condylar process of the mandible below, and the articular fossa (or glenoid fossa) of the temporal bone above. Between these articular surfaces is the articular disc (or meniscus), which is a biconcave, transversely oval disc composed of dense fibrous connective tissue. Each TMJ is covered by a fibrous capsule. There are tight fibers connecting the mandible to the disc, and loose fibers which connect the disc to the temporal bone, meaning there are in effect 2 joint capsules, creating an upper joint space and a lower joint space, with the articular disc in between. The synovial membrane of the TMJ lines the inside of the fibrous capsule apart from the articular surfaces and the disc. This membrane secretes synovial fluid, which is both a lubricant to fill the joint spaces, and a means to convey nutrients to the tissues inside the joint. Behind the disc is loose vascular tissue termed the "bilaminar region" which serves as a posterior attachment for the disc and also fills with blood to fill the space created when the head of the condyle translates down the articular eminence. Due to its concave shape, sometimes the articular disc is described as having an anterior band, intermediate zone and a posterior band. When the mouth is opened, the initial movement of the mandibular condyle is rotational, and this involves mainly the lower joint space, and when the mouth is opened further, the movement of the condyle is translational, involving mainly the upper joint space. This translation movement is achieved by the condylar head sliding down the articular eminence, which constitutes the front border of the articular fossa. The function of the articular eminence is to limit the forwards movement of the condyle. The ligament directly associated with the TMJ is the temporomandibular ligament, also termed the lateral ligament, which really is a thickening of the lateral aspect of the fibrous capsule. The stylomandibular ligament and the sphenomandibular ligament are not directly associated with the joint capsule. Together, these ligaments act to restrict the extreme movements of the joint. The muscles of mastication are paired on each side and work together to produce the movements of the mandible. The main muscles involved are the masseter, temporalis and medial and lateral pterygoid muscles. They can be thought of in terms of the directions they move the mandible, with most being involved in more than one type of movement due to the variation in the orientation of muscle fibers within some of these muscles. Each lateral pterygoid muscle is composed of 2 heads, the upper or superior head and the lower or inferior head. The lower head originates from the lateral surface of the lateral pterygoid plate and inserts at a depression on the neck of mandibular condyle, just below the articular surface, termed the pterygoid fovea. The upper head originates from the infratemporal surface and the infratemporal crest of the greater wing of the sphenoid bone. The upper head also inserts at the fovea, but a part may be attached directly to the joint capsule and to the anterior and medial borders of the articular disc. The 2 parts of lateral pterygoid have different actions. The lower head contracts during mouth opening, and the upper head contracts during mouth closing. The function of the lower head is to steady the articular disc as it moves back with the condyle into the articular fossa. It is relaxed during mouth closure. Noises from the TMJs are a symptom of dysfunction of these joints. The sounds commonly produced by TMD are usually described as a "click" or a "pop" when a single sound is heard and as "crepitation" or "crepitus" when there are multiple, grating, rough sounds. Most joint sounds are due to internal derangement of the joint, which is a term used to describe instability or abnormal position of the articular disc. Clicking often accompanies either jaw opening or closing, and usually occurs towards the end of the movement. The noise indicates that the articular disc has suddenly moved to and from a temporarily displaced position (disk displacement with reduction) to allow completion of a phase of movement of the mandible. If the disc displaces and does not reduce (move back into position) this may be associated with locking. Clicking alone is not diagnostic of TMD since it is present in high proportion of the general population, mostly in people who have no pain. Crepitus often indicates arthritic changes in the joint, and may occur at any time during mandibular movement, especially lateral movements. Perforation of the disc may also cause crepitus. Due to the proximity of the TMJ to the ear canal, joint noises are perceived to be much louder to the individual than to others. Often people with TMD are surprised that what sounds to them like very loud noises cannot be heard at all by others next to them. However, it is occasionally possible for loud joint noises to be easily heard by others in some cases and this can be a source of embarrassment e.g. when eating in company. Pain symptoms in TMD can be thought of as originating from the joint (arthralgia), or from the muscles (myofascial), or both. There is a poor correlation between TMD pain severity and evidence of tissue pathology. Generally, degenerative joint changes are associated with greater pain. Pain originating from the muscles of mastication as a result of abnormal muscular function or hyperactivity. The muscular pain is frequently, but not always, associated with daytime clenching or nocturnal bruxism. Sometimes TMD pain can radiate or be referred from its cause (i.e. the TMJ and/or the muscles of mastication) and be felt as headaches, earache or toothache. Due to the proximity of the ear to the temporomandibular joint, TMJ pain can often be confused with ear pain. The pain may be referred in around half of all patients and experienced as otalgia (earache). Conversely, TMD is an important possible cause of secondary otalgia. Treatment of TMD may then significantly reduce symptoms of otalgia and tinnitus, as well as atypical facial pain. Despite some of these findings, some researchers question whether TMJD therapy can reduce symptoms in the ear, and there is currently an ongoing debate to settle the controversy. The jaw deviates to the affected side during opening, and restricted mouth opening usually signifies that both TMJs are involved, but severe trismus rarely occurs. If the greatest reduction in movement occurs upon waking then this may indicate that there is concomitant sleep bruxism. In other cases the limitation in movement gets worse throughout the day. The jaw may lock entirely. Limitation of mandibular movement itself may lead to further problems involving the TMJs and the muscles of mastication. Changes in the synovial membrane may lead to a reduction in lubrication of the joint and contribute to degenerative joint changes. The muscles become weak, and fibrosis may occur. All these factors may lead to a further limitation of jaw movement and increase in pain. Degenerative joint disease, such as osteoarthritis or organic degeneration of the articular surfaces, recurrent fibrous and/or bony ankylosis, developmental abnormality, or pathologic lesions within the TMJ. Myofascial pain syndrome.][ In people with TMD, it has been shown that the lower head of lateral pterygoid contracts during mouth closing (when it should relax), and is often tender to palpation. To theorize upon this observation, some have suggested that due to a tear in the back of the joint capsule, the articular disc may be displaced forwards (anterior disc displacement), stopping the upper head of lateral pterygoid from acting to stabilize the disc as it would do normally. As a biologic compensatory mechanism, the lower head tries to fill this role, hence the abnormal muscle activity during mouth closure. There is some evidence that anterior disc displacement is present in proportion of TMD cases. Anterior disc displacement with reduction refers to abnormal forward movement of the disc during opening which reduces upon closing. Anterior disc displacement without reduction refers to an abnormal forward, bunched-up position of the articular disc which does not reduce. In this latter scenario, the disc is not intermediary between the condyle and the articular fossa as it should be, and hence the articular surfaces of the bones themselves are exposed to a greater degree of wear (which may predispose to osteoarthritis in later life). The general term "degenerative joint disease" refers to arthritis (both osteoarthritis and rheumatoid arthritis) and arthrosis. The term arthrosis may cause confusion since in the specialized TMD literature it means something slightly different to the wider medical literature. In medicine generally, arthrosis can be a nonspecific term for a joint, any disease of a joint (or specifically degenerative joint disease), and is also used as a synonym for osteoarthritis. In the specialized literature that has evolved around TMD research, arthrosis is differentiated from arthritis by the presence of low and no inflammation respectively. Both are however equally degenerative. The TMJs are sometimes described as one of the most used joints in the body. Over time, either with normal use or with parafunctional use of the joint, wear and degeneration can occur, termed osteoarthritis. Rheumatoid arthritis, an autoimmune joint disease, can also affect the TMJs. Degenerative joint diseases may lead to defects in the shape of the tissues of the joint, limitation of function (e.g. restricted mandibular movements), and joint pain. TMD is a symptom complex (i.e. a group of symptoms occurring together and characterizing a particular disease), which is thought to be caused by multiple, poorly understood factors, but the exact etiology is unknown. There are factors which appear to predispose to TMD (genetic, hormonal, anatomical), factors which may precipitate it (trauma, occlusal changes, parafunction), and also factors which may prolong it (stress and again parafunction). Overall, 2 hypotheses have dominated research into the causes of TMD, namely a psychosocial model and a theory of occlusal dysharmony. Interest in occlusal factors as a causative factor in TMD was especially widespread in the past, and the theory has since fallen out of favor and become controversial due to lack of evidence. Emotional stress (anxiety, depression, anger) may increase pain by causing autonomic, visceral and skeletal activity and by reduced inhibition via the descending pathways of the limbic system. The interactions of these biological systems have been described as a vicious "anxiety-pain-tension" cycle which is thought to be frequently involved in TMD. Put simply, stress and anxiety cause grinding of teeth and sustained muscular contraction in the face. This produces pain which causes further anxiety which in turn causes prolonged muscular spasm at trigger points, vasoconstriction, ischemia and release of pain mediators. The pain discourages use of the masticatory system (a similar phenomenon in other chronic pain conditions is termed "fear avoidance" behavior), which leads to reduced muscle flexibility, tone, strength and endurance. This manifests as limited mouth opening and a sensation that the teeth are not fitting properly. Persons with TMD have a higher prevalence of psychological disorders than people without TMD. People with TMD have been shown to have higher levels of anxiety, depression, somatization and sleep deprivation, and these could be considered important risk factors for the development of TMD. In the 6 months before the onset, 50-70% of people with TMD report experiencing stressful life events (e.g. involving work, money, health or relationship loss). It has been postulated that such events induce anxiety and causes increased jaw muscle activity. Muscular hyperactivity has also been shown in people with TMD whilst taking examinations or watching horror films. Others argue that a link between muscular hyperactivity and TMD has not been convincingly demonstrated, and that emotional distress may be more of a consequence of pain rather than a cause. Bruxism is an oral parafunctional activity where there is excessive clenching and grinding of the teeth. It can occur during sleep or whilst awake. The cause of bruxism itself is not completely understood, but psychosocial factors appear to be implicated in awake bruxism and dominergic dysfunction and other central nervous system mechanisms may be involved in sleep bruxism. If TMD pain and limitation of mandibular movement are greatest upon waking, and then slowly resolve throughout the day, this may indicate sleep bruxism. Conversely, awake bruxism tends to cause symptoms that slowly get worse throughout the day, and there may be no pain at all upon waking. The relationship of bruxism with TMD is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD.][][][ Indeed, the symptoms of TMD overlap with those of bruxism. Others suggest that there is no strong association between TMD and bruxism.][ A systematic review investigating the possible relationship concluded that when self reported bruxism is used to diagnose bruxism, there is a positive association with TMD pain, and when more strict diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower. Self reported bruxism is probably a poor method of identifying bruxism. There are also very many people who grind their teeth and who do not develop TMD. Bruxism and other parafunctional activities may play a role in perpetuating symptoms in some cases. Other parafunctional habits such as pen chewing, lip and cheek biting (which may manifest as morsicatio buccarum and/or linea alba), are also suggested to contribute to the development of TMD. Jaw thrusting, excessive gum chewing, nail biting, eating very hard foods. A majority of TMJD patients believe bruxism to be a contributory factor.][ Trauma, both micro and macrotrauma, is sometimes identified as a possible cause of TMD, however the evidence is not strong. Prolonged mouth opening (hyper-extension) is also suggested as a possible cause. It is thought that this leads to microtrauma and subsequent muscular hyperactivity. This may occur during dental treatment, with oral intubation whilst under a general anesthetic, during singing or wind instrument practice (really these can be thought of as parafunctional activities). Damage may be incurred during violent yawning, laughing, road traffic accidents, sports injuries, interpersonal violence, or during dental treatment, (such as tooth extraction). It has been proposed that a link exists between whiplash injuries (sudden neck hyper-extension usually occurring in road traffic accidents), and the development of TMD. This has been termed "post-traumatic TMD", to separate it from "idiopathic TMD". Despite multiple studies having been performed over the years, the cumulative evidence has been described as conflicting, with moderate evidence that TMD can occasionally follow whiplash injury. The research that suggests a link appears to demonstrate a low to moderate incidence of TMD following whiplash injury, and that pTMD has a poorer response to treatment than TMD which has not developed in relation to trauma. Occlusal factors as an etiologic factor in TMD is a controversial topic. Abnormalities of occlusion (problems with the bite) are often blamed for TMD but there is no evidence that these factors are involved. Occlusal abnormalities are incredibly common, and most people with occlusal abnormalities do not have TMD. Although occlusal features may affect observed electrical activity in masticatory muscles, there are no statistically significant differences in the number of occlusal abnormalities in people with TMD and in people without TMD. There is also no evidence for a causal link between orthodontic treatment and TMD. The modern, mainstream view is that the vast majority of people with TMD, occlusal factors are not related. Theories of occlusal factors in TMD are largely of historical interest. A causal relationship between occlusal factors and TMD was championed by Ramfjord in the 1960s. A small minority of dentists continue to prescribe occlusal adjustments in the belief that this will prevent or treat TMD despite the existence of systematic reviews of the subject which state that there is no evidence for such practices, and the vast majority of opinion being that no irreversible treatment should be carried out in TMD (see Occlusal adjustment). TMD does not obviously run in families like a genetic disease. It has been suggested that a genetic predisposition for developing TMD (and chronic pain syndromes generally) could exist. This has be postulated to be explained by variations of the gene which codes for the enzyme catechol-O-methyl transferase (COMT) which may produce 3 different phenotypes with regards pain sensitivity. COMT (together with monoamine oxidase) is involved in breaking down catecholamines (e.g. dopamine, epinephrine, and norepinephrine). The variation of the COMT gene which produces less of this enzyme is associated with a high sensitivity to pain. Females with this variation, are at 2-3 times greater risk of developing TMD than females without this variant. However this theory is controversial since there is conflicting evidence that appears to contradict it. Since females are more often affected by TMD than males, the female sex hormone estrogen has been suggested to be involved. The results of one study suggested that the periods of highest pain in TMD can be correlated with rapid periods of change in the circulating estrogen level. Low estrogen was also correlated to higher pain. In the menstrual cycle, estrogen levels fluctuate rapidly during ovulation, and also rapidly increases just before menstruation and rapidly decreases during menstruation. Post-menopausal females who are treated with hormone replacement therapy are more likely to develop TMD, or may experience an exacerbation if they already had TMD. Several possible mechanisms by which estrogen might be involved in TMD symptoms have been proposed. Estrogen may play a role in modulating joint inflammation, nocieceptive neurons in the trigeminal nerve, muscle reflexes to pain and μ-opioid receptors. TMD has been suggested to be associated with other conditions or factors, with varying degrees evidence and some more commonly than others. E.g. It has been shown that 75% of people with TMD could also be diagnosed with fibromyalgia, since they met the diagnostic criteria, and that conversely, 18% of people with fibromyalgia met diagnostic criteria for TMD. A possible link between many of these chronic pain conditions has been hypothesized to be due to shared pathophysiological mechanisms, and they have been collectively termed "central sensitivity syndromes", although other apparent associations cannot be explained in this manner. Group I: muscle disorders Ia. Myofascial pain: Ib. Myofascial pain with limited opening: Group II: disc displacements IIa. Disc displacement with reduction: IIb. Disc displacement without reduction with limited opening: IIc. Disc displacement without reduction, without limited opening: Group III: arthralgia, osteoarthritis, osteoarthrosis IIIa. Arthralgia: IIIb. Osteoarthritis of the TMJ: IIIc. Osteoarthrosis of the TMJ: Pain is the most common reason for people with TMD to seek medical advice. Joint noises may require auscultation with a stethescope to detect. Clicks of the joint may also be palpated, over the joint itself in the preauricular region, or via a finger inserted in the external acoustic meatus, which lies directly behind the TMJ. The differential diagnosis is with degenerative joint disease (e.g. osteoarthritis), rheumatoid arthritis, temporal arteritis, otitis media, parotitis, mandibular osteomyelitis, Eagle syndrome, trigeminal neuralgia,][ oromandibular dystonia,][ deafferentation pains, and psychogenic pain. Various diagnostic systems have been described. Some consider the Research Diagnostic Criteria method the gold standard. Abbreviated to "RDC/TMD", this was first introduced in 1992 by Dworkin and LeResche in an attempt to classify temporomandibular disorders by etiology and apply universal standards for research into TMD. This method involves 2 diagnostic axes, namely axis I, the physical diagnosis, and axis II, the psychologic diagnosis. Axis I contains 3 different groups which can occur in combinations of 2 or all 3 groups, (see table). McNeill 1997 described TMD diagnostic criteria as follows: The International Headache Society's diagnostic criteria for "headache or facial pain attributed to temporomandibular joint disorder" is similar to the above: TMD can be difficult to manage, and since the disorder transcends the boundaries between several health-care disciplines — in particular, dentistry and neurology, the treatment may often involve multiple approaches and be multidisciplinary. Most who are involved in treating and researching TMD now agree that any treatment carried out should not permanently alter the jaw or teeth, and should be reversible. To avoid permanent change, over-the-counter or prescription pain medications may be prescribed. Given the important role that psychosocial factors appear to play in TMD, psychosocial interventions could be viewed to be central to the management. There is a suggestion that treatment of factors that modulate pain sensitivity such as mood disorders, anxiety and fatigue, may be important in the treatment of TMD, which often tends to attempt to address the pain directly. Cognitive Behavioral Therapy (CBT) has been used in TMD and has been shown to be efficacious by meta analyses. Hypnosis is suggested by some to be appropriate for TMD. Studies have suggested that it may even be more beneficial than occlusal splint therapy, and has comparable effects to relaxation techniques. Relaxation techniques include progressive muscle relaxation, yoga, and meditation. It has been suggested that TMD involves increased sensitivity to external stimuli leading to an increased sympathetic (fight or flight) response with cardiovascular and respiratory alterations. Relaxation techniques cause reduced sympathetic activity, including muscle relaxation and reducing sensitivity to external stimuli, and provoke a general sense of well being and reduced anxiety. Occlusal splints (also termed bite plates or intra-oral appliances) are often used by dentists to treat TMD. They are usually made of acrylic and can be hard or soft. They can be designed to fit onto the upper teeth or the lower teeth. They may cover all the teeth in one arch (full coverage splint) or only some (partial coverage splint). Splints are also termed according to their intended mechanism, such as the anterior positioning splint or the stabilization splint. Although occlusal splints are generally considered a reversible treatment, sometimes partial coverage splints lead to pathologic tooth migration (changes in the position of teeth). Normally splints are only worn during sleep, and therefore probably do nothing for people who engage in parafunctional activities during wakefulness rather than during sleep. There is slightly more evidence for the use of occlusal splints in sleep bruxism than in TMD. At the least, they will mechanically protect the teeth from pathologic tooth wear associated with bruxism. A splint can also have a diagnostic role if it demonstrates excessive occlusal wear after a period of wearing it each night. This may confirm the presence of sleep bruxism if it was in doubt. Soft splints are occasionally reported to worsen discomfort related to TMD. Specific types of occlusal splint are discussed below. A stabilization splint is a hard acrylic splint that forces the teeth to meet in an "ideal" relationship for the muscles of mastication and the TMJs. It is claimed that this technique reduces abnormal muscular activity and promotes "neuromuscular balance". A stabilization splint is only intended to be used for about 2–3 months. It is more complicated to construct than other types of splint since a face bow record is required and significantly more skill on the part of the dental technician. This kind of splint should be properly fitted to avoid exacerbating the problem and used for brief periods of time. The use of the splint should be discontinued if it is painful or increases existing pain. A systematic review of all the scientific studies investigating the efficacy of stabilization splints concluded the following: "On the basis of our analysis we conclude that the literature seems to suggest that there is insufficient evidence either for or against the use of stabilization splint therapy over other active interventions for the treatment of TMD. However, there is weak evidence to suggest that the use of stabilization splints for the treatment of TMD may be beneficial for reducing pain severity, at rest and on palpation, when compared to no treatment". Partial coverage splints are recommended by some experts, but they have the potential to cause unwanted tooth movements, which rarely can be severe. The mechanism of this tooth movement is that the splint effectively holds some teeth out of contact and puts all the force of the bite onto the teeth which the splint covers. This can cause the covered teeth to be intruded, and those that are not covered to over-erupted. I.e. a partial coverage splint can act as a Dahl appliance. Examples of partial coverage splints include the NTI-TSS ("nociceptive trigeminal inhibitor tension suppression system"), which covers the upper front teeth only. Due to the risks involved with long term use, some discourage the use of any type of partial coverage splint. An anterior positioning splint is a splint that designed to promote an anteriorly displaced disc. It is rarely used. A 2010 review of all the scientific studies carried out to investigate the use of occlusal splints in TMD concluded: "Hard stabilization appliances, when adjusted properly, have good evidence of modest efficacy in the treatment of TMD pain compared to non-occluding appliances and no treatment. Other types of appliances, including soft stabilization appliances, anterior positioning appliances, and anterior bite appliances, have some RCT evidence of efficacy in reducing TMD pain. However, the potential for adverse events with these appliances is higher and suggests the need for close monitoring in their use." Medication is the main method of managing pain in TMD, mostly because there is little if any evidence of the effectiveness of surgical or dental interventions. Many different drugs have been used to treat TMD pain, such as analgesics (pain killers), benzodiazepines (e.g. clonazepam, prazepam, diazepam), anticonvulsants (e.g. gabapentin), muscle relaxants (e.g. cyclobenzaprine), and others. Analgesics that have been studied in TMD include non-steroidal anti-inflammatory drugs (e.g. piroxicam, diclofenac, naproxen) and cyclo-oxygenase-2 inhibitors (e.g. celecoxib). Topical methyl salicylate and topical capsaicin have also been used. Other drugs that have been described for use in TMD include glucosamine hydrochloride/chondroitin sulphate and propranolol. Despite many randomized control trials being conducted on these commonly used mediciations for TMD a systematic review carried out in 2010 concluded that was insufficient evidence to support or not to support the use of these drugs in TMD. Low-doses of anti-muscarinic tricyclic antidepressants such as amitriptyline, or nortriptyline have also been described. In a subset of people with TMD who are not helped by either noninvasive and invasive treatments, long term use of opiate analgesics has been suggested, although these drugs carry a risk of drug dependence and other side effects. Examples include morphine, fentanyl, oxycodone, tramadol, hydrocodone, and methadone. Botulinum toxin solution ("Botox") is sometimes used to treat TMD. Injection of botox into the lateral pterygoid muscle has been investigated in multiple randomized control trials, and there is evidence that it is of benefit in TMD. It is theorized that spasm of lateral pterygoid causes anterior disc displacement. Botulinum toxin causes temporary muscular paralysis by inhibiting acetylcholine release at the neuromuscular junction. The affects usually last for a period of months before they wear off. Complications include the creation of a "fixed" expression due to diffusion of the solution and subsequent involvement of the muscles of facial expression, which lasts until the affects of the botox wear off. Injections of local anesthetic, sometimes combined with steroids, into the muscles (e.g. the temoralis muscle or its tendon) are also sometimes used. Local anesthetics may provide temporary pain relief, and steroids inhibit pro-inflammatory cytokines. Steroids and other medications are sometimes injected directly into the joint (See Intra-articular injections). Physiotherapy (physical therapy) is sometimes used as a adjuvant to other methods of treatment in TMD. There are many different approaches described, but exercises aiming to increase the range of mandibular movements are commonly involved. Jaw exercises aim to directly oppose the negative effects of disuse that may occur in TMD, due to pain discouraging people from moving their jaw. After initial instruction, people are able to perform a physical therapy regimen at home. The most simple method is by regular stretching within pain tolerance, using the thumb and a finger in a "scissor" maneuver. Gentle force is applied until pain of resistance is felt, and then the position is held for several seconds. Commercial devices have been developed to carry out this stretching exercise (e.g. the "Therabite" appliance). Over time, the amount of mouth opening possible without pain can be gradually increased. A baseline record of the distance at the start of physical therapy (e.g. the number of fingers that can be placed vertically between the upper and lower incisors), can chart any improvement over time. It has been suggested that massage therapy for TMD improves both the subjective and objective health status. "Friction massage" uses surface pressure to causes temporary ischemia and subsequent hyperemia in the muscles, and this is hypothesized to inactivate trigger points and disrupt small fibrous adhesions with in the muscle that have formed following surgery or muscular shortening due to restricted movement. Occasionally physiotherapy for TMD may include the use of transcutaneous electrical nerve stimulation (TENS), which may override pain by stimulation of superficial nerve fibers and lead to pain reduction which extends after the time where the TENS is being actually being applied, possibly due to release of endorphins. Others recommend the use of ultrasound, theorized to produce tissue heating, alter blood flow and metabolic activity at a level that is deeper than possible with surface heat applications. Low level laser therapy a controversial treatment using lasers at levels which do not kill cells within the target tissues. "Laser photobiomodulation" is theorized to reduce TMD pain and give anti-inflammatory effects. The mechanisms of action are not thought to be related to the generation of heat in the tissue, but rather via a promotion of cellular and tissue alterations which increase the recovery and healing potential of the tissue, triggered by metabolic activation (e.g. increased sodium potassium pump mitochondrial activity, increased vascularization, and fibroblast formation). Low level laser therapy may be effective in reducing TMD pain. There is some evidence that some people who use nighttime biofeedback to reduce nighttime clenching experience a reduction in TMD. This is the adjustment or reorganizing of the existing occlusion, carried out in the belief that this will redistribute forces evenly across the dental arches and/or achieve a more favorable position of the condyles in the fossae, which is purported to lessen tooth wear, bruxism and TMD, but this is controversial. These techniques are sometimes termed "occlusal rehabilitation" or "occlusal equilibration". At its simplest, occlusal adjustment involves selective grinding (with a dental drill) of the enamel of the occlusal surfaces of teeth, with the aim of allowing the upper teeth to fit with the lower teeth in a more harmonious way. However, there is much disagreement between proponents of these techniques on most of the aspects involved, including the indications and the exact goals. Occlusal adjustment can also be very complex, involving orthodontics, restorative dentistry or even orthognathic surgery. Some have criticized these occlusal reorganizations as having no evidence base, and irreversibly damaging the dentition on top of the damage already caused by bruxism. A "middle ground" view of these techniques is that occlusal adjustment in most cases of TMD is neither desirable nor helpful as a first line treatment, and furthermore, with few exceptions, any adjustments should be reversible. However, most dentists consider this unnecessary overtreatment, with no evidence of benefit. Specifically, orthodontics and orthognathic surgery are not considered by most to be appropriate treatments for TMD. A systematic review investigating all the scientific studies carried out on occlusal adjustments in TMD concluded the following: "There is an absence of evidence of effectiveness for occlusal adjustment. Based on these data occlusal adjustment cannot be recommended for the treatment or prevention of TMD. These conclusions were based largely on the fact that, despite many different scientific studies investigating this measure as a therapy, overall no statistically significant differences can be demonstrated between treatment with occlusal adjustment and treatment with placebo. The reviewers also stated that there are ethical implications if occlusal adjustment was found to be ineffective in preventing TMD. Orthodontic treatment, as described earlier, is sometimes listed as a possible predisposing factor in the development of TMD. On the other hand, orthodontic treatment is also often carried out in the belief that it may treat or prevent TMD. Another systematic review investigating the relationship between orthodontics and TMD concluded the following: "There is no evidence to support or refute the use of orthodontic treatment for the treatment of TMD. In addition, there are no data which identify a link between active orthodontic intervention and the causation of TMD. Based on the lack of data, orthodontic treatment cannot be recommended for the treatment or prevention of TMD." A common scenario where a newly placed dental restoration (e.g. a crown or a filling) is incorrectly contoured, and creates a premature contact in the bite. This may localize all the force of the bite onto one tooth, and cause inflammation of the periodontal ligament and reversible increase in tooth mobility. The tooth may become tender to bite on. Here, the "occlusal adjustment" has already taken place inadvertently, and the adjustment aims to return to the pre-existing occlusion. This should be distinguished from attempts to deliberately reorganize the native occlusion. Attempts in the last decade to develop surgical treatments based on MRI and CAT scans now receive less attention. These techniques are reserved for the most difficult cases where other therapeutic modalities have failed. The American Society of Maxillofacial Surgeons recommends a conservative/non-surgical approach first. Only 20% of patients need to proceed to surgery. Examples of surgical procedures that are used in TMD, some more commonly than others, include arthrocentesis, arthroscopy, menisectomy, disc repositioning, condylotomy or joint replacement. Invasive surgical procedures in TMD may cause symptoms to worsen. Menisectomy, also termed discectomy refers to surgical removal of the articular disc. This is rarely carried out in TMD, it may have some benefits for pain, but dysfunciton may persist and overall there it leads to degeneration or remodeling of the TMJ. TMJ arthrocentesis refers to lavage (flushing out) of the upper joint space (where most of the translation movement takes place) with saline via the introduction of cannulae. It is theorized that the hydraulic pressure generated within the joint combined with external manipulation is capable of releasing adhesions or the anchored disc phenomenon and leads to an improvement in the movement ("lysis and lavage"). It is also suggested that undesirable contents within the synovial fluid of the joint can be washed out, such as microscopic debris (from breakdown of the articular surfaces) and pain mediators (enzymes and prostaglandins), and there is also stimulation of the synovial membrane to restore its normal lubricating function. It was initially used to treat acute closed lock, however it has since come to be used chronic closed lock, chronic anterior displaced disc with reduction, and degenerative joint disease (e.g. arthritis). In acute closed lock, it is theorized that the upper joint space is inflated from its normally collapsed state during this procedure, and this extra space frees up the articular disc which returns to its correct position. This is the least invasive, and easiest to carry out of the surgical options. It can be carried out under local anesthetic (and for this reason is cheaper than arthroscopy, although it is also carried out under general anesthetic) and has minimal complications. Although it has been suggested that arthrocentesis decreases pain, increases maximal incisal opening and has prolonged affects, when the procedure was investigated by a systematic review, the impact on pain was comparable to arthroscopy and the results are unstable. The review concluded by suggesting that arthrocentesis only be used for TMD within well designed randomized controlled trial (i.e. for the purposes of further research and not for routine management). Arthrocentesis may be combined with injection of sodium hyaluronate into the joint at the end of the lavage with the aim to improve lubrication within the joint. Arthroscopy involves the introduction of an arthroscope (a very thin, flexible camera) into the joint via single cannula (as opposed to arthrocentesis which usually involves 2 cannulae and no arthroscope), allowing the joint space to be visualized on a monitor and explored by the surgeon. Arthroscopy is also used in other joints and the technique is similar to laparoscopy. The cannula is inserted via a small incision just in front of the ear. The arthroscope has a built in capacity to pump in or suck out saline. Arthroscopy may be intended as a purely diagnostic procedure, or it may be employed in combination with surgical interventions within the joint, in which case a second "working" cannula is also inserted into the joint. Examples include release of adhesions (e.g. by blunt dissection or with a laser) or release of the disc. Biopsies or disc reduction can also be carried out during arthroscopy. Arthroscopy is usually carried out under general anesthesia. Arthroscopy has advantages over arthrocentesis in that it allows for detection of problems inside the joint such as perforation or synovitis. As with arthrocentesis, the procedure may be combined with sodium hyaluronate injection into the joint at the end of the procedure. Both sodium hyaluronate and glucocorticoids have been injected into the joints in order to treat TMD. Sodium hyaluronate is a component of the normal synovial fluid that fills the joint spaces in health. Its function is to lubricate and maintain the internal environment of the joint. It has been used for arthritis in the knee and hip joints, and it was first used for TMD in 1985. A systematic review found that hyaluronate might be beneficial for clinical TMD signs in the long term, but that this may be unstable. The effects of hyaluronate may be similar to glucocorticoids. There may be added benefit in arthrocentesis or arthroscopy if intra-articular injections are combined with these procedures. Reported adverse events are minor and temporary. Acupuncture is sometimes used for TMD. A systematic review carried out in 2011 concluded that there was limited evidence of benefit for acupuncture as a symptomatic treatment for TMD. A short term reduction in muscular pain of muscular origin can usually be observed after acupuncture in TMD, which is more than observed for placebo treatment. Other sources suggest that acupuncture is best employed as an adjuvent to other treatments in TMD, and that the long term efficacy of acupuncture for TMD is unknown. There are no reported adverse events of acupuncture when used for TMD, so it could be considered a reversible treatment. Practitioners of chiropractic medicine sometimes carry out chiropractic adjustments (also termed manipulations or mobilizations) in the belief that this will treat TMD. Related conditions that are also claimed to be treatable by chiropractic include tension headaches and neck pain. Some sources suggest that there is some evidence of efficacy of chiropractic treatment in TMD, but the sources cited for these statements were case reports and a case series of only 9 participants. Multiple, large randomized control trials and independent meta analyses are required to properly asses the efficacy of a treatment in evidence based medicine. One review concluded "inconclusive evidence in a favorable direction regarding mobilization and massage for TMD". Overall, although there is general agreement that chiropractic may be of comparable benefit to other manual therapies for lower back pain, there is no credible evidence of efficacy in other conditions, including TMD. However, there is some evidence of possible adverse effects from cervical (neck) vertebral manipulation, which sometimes may be serious. It has been suggested that the natural history of TMD is benign and self-limiting, with symptoms slowly improving and resolving over time. The prognosis is therefore good. However, the persistent pain symptoms, psychological discomfort, physical disability and functional limitations may detriment quality of life. It has been suggested that TMD does not cause permanent damage and does not progress to arthritis in later life, however degenerative disorders of the TMJ such as osteoarthritis are included within the spectrum of TMDs in some classifications. TMD mostly affects people in the 20 - 40 age group, and the average age is 33.9 years. People with TMD tend to be younger adults, who are otherwise healthy. Within the catchall umbrella of TMD, there are peaks for disc displacements at age 30, and for inflammatory-degenerative joint disorders at age 50. About 75% of the general population may have at least one abnormal sign associated with the TMJ (e.g. clicking), and about 33% have at least one symptom of TMD. However, only in 3.6-7% will this be of sufficient severity to trigger the individual to seek medical advice. For unknown reasons, females are more likely to be affected than males, in a ratio of about 2:1, although others report this ratio to be as high as 9:1. Females are more likely to request treatment for TMD, and their symptoms are less likely to resolve. Females with TMD are more likely to be nulliparous than females without TMD. It has also been reported that female caucasians are more likely to be affected by TMD, and at an earlier age, than female African Americans. According to the most recent analyses of epidemiologic data using the RDC/TMD diagnostic criteria, of all TMD cases, group I (muscle disorders) accounts for 45.3%, group II (disc displacements) 41.1%, and group III (joint disorders) 30.1% (individuals may have diagnoses from more than one group). Using the RDC/TMD criteria, TMD has a prevelence in the general population of 9.7% for group I, 11.4% for group IIa, and 2.6% for group IIIa. Temporomandibular disorders were described as early as ancient Egypt. An older name for the condition is "Costen's syndrome", eponymously referring to James B. Costen. Costen was an otolaryngologist, and although he was not the first physician to describe TMD, he wrote extensively on the topic, starting in 1934, and was the first to approach the disorder in an integrated and systematic way. Costen hypothesized that malocclusion caused TMD, and placed emphasis on ear symptoms, such as tinnitus, otaglia, impaired hearing, and even dizziness. Specifically, Costen believed that the cause of TMD was mandibular over-closure, recommending a treatment revolving around building up the bite. The eponym "Costen syndrome" became commonly used shortly after his initial work, but in modern times it has been dropped, partially because occlusal factors are now thought to play little, if any, role in the development of TMD, and also because ear problems are now thought to be less associated with TMD. Other historically important terms that were used for TMD include "TMJ disease" or "TMJ syndrome", which are now rarely used. M: MOU anat/devp noco/cofa (c)/cogi/tumr, sysi proc (peri), drug (A1)
A crown is a type of dental restoration which completely caps or encircles a tooth or dental implant. Crowns are often needed when a large cavity threatens the ongoing health of a tooth. They are typically bonded to the tooth using a dental cement. Crowns can be made from many materials, which are usually fabricated using indirect methods. Crowns are often used to improve the strength or appearance of teeth. While inarguably beneficial to dental health, the procedure and materials can be relatively expensive. The most common method of crowning a tooth involves using a dental impression of a prepared tooth by a dentist to fabricate the crown outside of the mouth. The crown can then be inserted at a subsequent dental appointment. Using this indirect method of tooth restoration allows use of strong restorative materials requiring time consuming fabrication methods requiring intense heat, such as casting metal or firing porcelain which would not be possible to complete inside the mouth. Because of the expansion properties, the relatively similar material costs, and the aesthetic benefits, many patients choose to have their crown fabricated with gold. As new technology and materials science has evolved, computers are increasingly becoming a part of crown and bridge fabrication, such as in CAD/CAM Dentistry. There are additional situations in which a crown would be the restoration of choice. Dental implants are placed into either the maxilla or mandible as an alternative to partial or complete edentulism. Once placed and properly integrated into the bone, implants may then be fitted with a number of different prostheses: When teeth undergo endodontic treatment, or root canal therapy, they are devitalized when the nerve and blood supply are cut off and the space which they previously filled, known as the "pulp chamber" and "root canal", are thoroughly cleansed and filled with various materials to prevent future invasion by bacteria. Although there may very well be enough tooth structure remaining after root canal therapy is provided for a particular tooth to restore the tooth with an intracoronal restoration, this is not suggested in most teeth. The vitality of a tooth is remarkable in its ability to provide the tooth with the strength and durability it needs to function in mastication. The living tooth structure is surprisingly resilient and can sustain considerable abuse without fracturing. Consequently, after root canal therapy is performed, a tooth becomes extremely brittle and is significantly weaker than its vital neighbors. The average person can exert 150–200 lbs (70-90 kg). of muscular force on his or her posterior teeth, which is approximately nine times the amount of force that can be exerted in the anterior. If the effective posterior contact area on a restoration is 0.1 mm², over 1 million PSI of stress is placed on the restoration. Therefore, posterior teeth (i.e. molars and premolars) should in almost all situations be crowned after undergoing root canal therapy to provide for proper protection against fracture (mandibular premolars, being very similar in crown morphology to canines, may in some cases be protected with intracoronal restorations). Should an endodontically treated tooth not be properly protected, there is a chance of it succumbing to breakage from normal functional forces. This fracture may well be difficult to treat, such as a "vertical root fracture" . Anterior teeth (i.e. incisors and canines), which are exposed to significantly lower functional forces, may effectively be treated with intracoronal restorations following root canal therapy if there is enough tooth structure remaining after the procedure. Another situation in which a crown is the restoration of choice is when a tooth is intended as an abutment tooth for a removable partial denture, but is initially unfavorable for such a task. If the abutment teeth onto which the RPD is supposed to clasp do not possess the proper dimensions or features required, these aspects can be built into what is known as a surveyed crown. A fourth situation in which a crown would be the restoration of choice is when a patient desires to have his or her smile aesthetically improved but when partial coverage (i.e., a veneer/laminate) is not an option for one or more reasons. If the patient's occlusion does not permit for a mildly-retentive restoration, or if there is too much decay or a fracture within the tooth structure, a porcelain or composite veneer may not be placed with any adequate guarantee for its durability. Similarly, a "bruxer" (someone who clenches or grinds their teeth) may produce enough force to repeatedly dislodge or irreversibly abrade any veneer a dentist can plan for. In such a case, full coverage crowns can alter the size, shape or shade of a patient's teeth while protecting against failure of the restoration. Makeover shows such as Extreme Makeover make extensive use of crowns, as the time-frame of the makeover is too short to allow up to 18 months for orthodontic treatment for problems that might otherwise be corrected more conservatively. Preparation of a tooth for a crown involves permanently removing much of the tooth's original structure, including portions that might still be healthy and structurally sound. All currently available materials for making crowns are not as good as healthy, natural tooth structure, so teeth should only be crowned when an oral health-care professional has evaluated the tooth and decided that the overall value of the crown will outweigh the disadvantage of needing to remove some healthy parts of the tooth. This can be a very complex evaluation to make, so different dentists (trained at different institutions, with different experiences, and trained in different methods of treatment planning and case selection) may come to different conclusions regarding treatment. Traditionally more than one visit is required to complete crown and bridge work, and the additional time required for the procedure can be a disadvantage; the increased benefits of such a restoration, however, will generally offset these considerations. When preparing a tooth for a traditional crown, the enamel may be totally removed and the finished preparation should, thus, exist primarily in dentin. As elaborated on below, the amount of tooth structure required to be removed will depend on the material(s) being used to restore the tooth. If the tooth is to be restored with a full gold crown, the restoration need only be .5 mm in thickness (as gold is very strong), and therefore, a minimum of only .5 mm of space needs to be made for the crown to be placed. If porcelain is to be applied to the gold crown, an additional minimum of 1 mm of tooth structure needs to be removed to allow for a sufficient thickness of the porcelain to be applied, thus bringing the total tooth reduction to minimally 1.5 mm. If there is not enough tooth structure to properly retain the traditional prosthetic crown, the tooth requires a build-up material. This can be accomplished with a pin-retained direct restoration, such as amalgam or a composite resin, or in more severe cases, may require a post and core. Should the tooth require a post and core, endodontic therapy would then be indicated, as the post descends into the devitalized root canal for added retention. If the tooth, because of its relative lack of exposed tooth structure, also requires crown lengthening, the total combined time, effort and cost of the various procedures, together with the decreased prognosis because of the combined inherent failure rates of each procedure, might make it more reasonable to have the tooth extracted and opt to have an implant placed. In recent years, the technological advances afforded by CAD/CAM dentistry offer viable alternatives to the traditional crown restoration in many cases. Where the traditional indirectly fabricated crown requires a tremendous amount of surface area to retain the normal crown, potentially resulting in the loss of healthy, natural tooth structure for this purpose, the all-porcelain CAD/CAM crown can be predictably used with significantly less surface area. As a matter of fact, the more enamel that is retained, the greater the likelihood of a successful outcome. As long as the thickness of porcelain on the top, chewing portion of the crown is 1.5mm thick or greater, the restoration can be expected to be successful. The side walls which are normally totally sacrificed in the traditional crown are generally left far more intact with the CAD/CAM option. In regards to post & core buildups, these are generally contraindicated in CAD/CAM crowns as the resin bonding materials do best bonding the etched porcelain interface to the etched enamel/dentin interfaces of the natural tooth itself. The crownlay is also an excellent alternative to the post & core buildup when restoring a root canal treated tooth. The prepared tooth also needs to possess 3 to 5 degrees of taper to allow for the restoration to be properly placed on the tooth. The taper should not exceed 20 degrees. Fundamentally, there can be no undercuts on the surface of the prepared tooth, as the restoration will not be able to be removed from the die, let alone fit on the tooth (see explanation of lost-wax technique below to understand of the processes involved in crown fabrication). At the same time, too much taper will severely limit the grip that the crown has on the prepared tooth, thus contributing to failure of the restoration. Generally, 6° of taper around the entire circumference of the prepared tooth, giving a combined taper of 12° at any given sagittal section through the prepared tooth, is appropriate to both allow the crown to fit yet provide enough grip. The most coronal position of untouched tooth structure (that is, the continual line of original, undrilled tooth structure at or near the gum line) is referred to as the margin. This margin will be the future continual line of tooth-to-restoration contact, and should be a smooth, well-defined delineation so that the restoration, no matter how it is fabricated, can be properly adapted and not allow for any openings visible to the naked eye, however slight. An acceptable distance from tooth margin to restoration margin is anywhere from 40-100 μm][. However, the R.V. Tucker method of gold inlay and onlay restoration produces tooth-to-restoration adaptation of potentially only 2 μm][, confirmed by scanning electron microscopy; this is less than the diameter of a single bacterium. Naturally, the tooth-to-restoration margin is an unsightly thing to have exposed on the visible surface of a tooth when the tooth exists in the aesthetic zone of the smile. In these areas, the dentist would like to place the margin as far apical (towards the root tip of the tooth) as possible, even below the gum line. While there is no issue, per se, with placing the margin at the gumline, problems may arise when placing the margin too subgingivally (below the gumline). First, there might be issues in terms of capturing the margin in an impression to make the stone model of the prepared tooth (see stone model replication of tooth in photographs, above). Secondly, there is the seriously important issue of biologic width. Biologic width is the mandatory distance to be left between the height of the alveolar bone and the margin of the restoration, and if this distance is violated because the margin is placed too subgingivally, serious repercussions may follow. In situations where the margin cannot be placed apically enough to provide for proper retention of the prosthetic crown on the prepared tooth structure, the tooth or teeth involved should undergo a crown lengthening procedure. There are a number of different types of margins that can be placed for restoration with a crown. There is the chamfer, which is popular with full gold restorations, which effectively removed the smallest amount of tooth structure. There is also a shoulder, which, while removing slightly more tooth structure, serves to allow for a thickness of the restoration material, necessary when applying porcelain to a PFM coping or when restoring with an all-ceramic crown (see below for elaboration on various types of crowns and their materials). When using a shoulder preparation, the dentist is urged to add a bevel; the shoulder-bevel margin serves to effectively decrease the tooth-to-restoration distance upon final cementation of the restoration. A very important consideration when restoring with a crown is the incorporation of the ferrule effect. As with the bristles of a broom, which are grasped by a ferrule when attached to the broomstick, the crown should envelop a certain height of tooth structure to properly protect the tooth from fracture after being prepared for a crown. This has been established through multiple experiments as a mandatory continuous circumferential height of 2 mm; any less provides for a significantly higher failure rate of endodontically-treated crown-restored teeth. When a tooth is not endodontically treated, the remaining tooth structure will invariably provide the 2 mm height necessary for a ferrule, but endodontically treated teeth are notoriously decayed and are often missing significant solid tooth structure. Because they are weaker after the additional removal of tooth structure that occurs during a root canal procedure, endodontically treated teeth require proper protection against vertical root fracture. Some have speculated that a shoulder preparation on an all ceramic crown that will be bonded in place may have the same effect as a ferrule. As crowns are fabricated indirectly (outside of the mouth) free of the encumbrances of saliva, blood, and tight quarters, they can be made to fit more precisely than restorative materials placed directly (inside the mouth). In regards to marginal adaptations (the circumferential seal which keeps bacteria out), anatomically correct contacts (touching adjacent teeth properly so food will not be retained), and proper morphology, the indirect fabrication of the restorations are unprecedented. Indirectly fabricated crowns may be fabricated one of two ways. In the traditional sense, the tooth in question is prepared, a mold is taken, a temporary crown is placed and then the patient leaves. The mold is then sent to a dental laboratory whereby a model is constructed from the mold, and a crown is created on the model (usually out of porcelain, ceramic, gold, or porcelain/ceramic fused to metal) to replace the missing tooth structure. The patient returns to the dental office a week or two later and then the temporary is removed and the crown is fitted and cemented in place. Alternatively, a crown may be indirectly fabricated utilizing technology and techniques relating to CAD/CAM dentistry, whereby the tooth is prepared and computer software is used to create a virtual restoration which is milled on the spot and bonded permanently in place an hour or two later. There are even restorations that fall between an onlay and a full crown when it comes to preservation of natural tooth structure. In the past, it was somewhat common to find dentists who prepared teeth for 3/4 and 7/8 crowns. Such restorations would generally be fabricated for maxillary second premolars or first molars, which might only be slightly visible when a patient smiled. Thus, the dentist would preserve healthy natural tooth structure that existed on the mesiobuccal corner of the tooth for aesthetic purposes, the remainder of the tooth would be enclosed in restorative material. Even when porcelain-fused-to-metal and all-ceramic crowns were developed, preserving any amount of tooth structure adds to the overall strength of the tooth. Some dentists feel that the structural benefits of retaining some of the original tooth structure are more than offset by the potential problems of having a significantly longer marginal length (the "seam" on the surface between the crown and the tooth). Inlays, onlays, porcelain veneers, crownlays and all varieties of crowns can also be fabricated out of ceramic materials, such as in CAD/CAM Dentistry or traditionally in a dental laboratory setting. CAD/CAM technology can allow for the immediate, same day delivery of these types restorations which are milled out of blocks of solid porcelain which matches the shade or color of the patients teeth. Traditionally, all-ceramic restorations have been made off site in a dental laboratory either out of feldspathic porcelains or pressed ceramics. This indirect method of fabrication involves molds and temporaries, but can yield quite beautiful end-results if communication between the laboratory and the dentist is sound. The greatest difference between these two differing modalities lies in the fact that the CAD/CAM route does not require temporization, while the laboratory-fabricated route does. Some argue that this lack of temporization can result in a decreased need for root canal therapy, as there is no temporary leakage between visits. Restorations that are all-ceramic require wide shoulder margins and reductions of at least 1.0 - 1.5 mm across the occlusal (chewing) surfaces of the teeth. There are times where this reduction would be considered excessive, just as there are times when previous restorations or pathology require this much removal or more. Arguments against using all-ceramic restorations include a greater chance of fracture, when little to no enamel remains for proper adhesive bonding, or potentially when the patient clenches or grinds their teeth ("bruxes") excessively. Indications for using all-ceramic restorations include more aesthetic results, when metal compatibility issues exist, and when removal of less tooth structure is desired. All-ceramic restorations do not require resistance and retention form and consequently less surface area need be removed and the restoration will still stay in place by virtue of micromechanical and chemical bonding. Ceramic materials such as lithium disilicate dental ceramics have recently been developed which provide greater strength and life-expectancy of dental restorations. Although no dental restoration lasts forever, the average lifespan of a crown is around 10 years. While this is considered comparatively favorable to direct restorations, they can actually last up to the life of the patient (50 years or more) with proper care. One reason why a 10 year lifespan is quoted is because a dentist can usually provide patients with this figure and be confident that a crown that the dental lab makes will last at least this long. Many dental insurance plans in North America will allow for a crown to be replaced after only five years. The most important factor affecting the lifespan of any restorative is the continuing oral hygiene of the patient. Other factors are the skill of the dentist and their lab technician, the material used and appropriate treatment planning and case selection. Full gold crowns last the longest, as they are fabricated as a single piece of gold. PFMs, or porcelain-fused-to-metal crowns possess an additional dimension in which they are prone to failure, as they incorporate brittle porcelain into their structure. Although incredibly strong in compression, porcelain is terribly fragile in tension, and fracture of the porcelain increases the risk of failure, which rises as the number of surfaces covered with porcelain is increased. A traditional PFM with occlusal porcelain (i.e. porcelain applied to the biting surface of a posterior tooth) has a 7% higher chance of failure per year than a corresponding full gold crown. When crowns are used to restore endodontically treated teeth, they reduce the likelihood of the tooth fracturing due to the brittle devitalized nature of the tooth and provide a better seal against invading bacteria. Although the inert filling material within the root canal blocks microbial invasion of the internal tooth structure, it is actually a superior coronal seal, or marginal adaptation of the restoration in or on the crown of the tooth, which prevents reinvasion of the root canal. The main disadvantages of restoration with a crown are extensive irreversible tooth preparation (grinding away) and higher costs than for direct restorations such as amalgam or dental composite. The benefits, as described above, include long-term durability and evidence-based success as compared to other restorations or no treatment. The crowning of two fairly large molars to sling a bridge between them for a missing tooth is a costly and sometimes oversold procedure. The increased food and bacteria trapping of the underside of the bridge often offsets the benefits of the bridge element in maintaining the positions of the opposing teeth and the loss of the ease of use and mouth feel of two big natural teeth.][ It is usually the damage to a tooth that dictates the need for a crown, and alternative treatments are usually less effective.][ Risks and benefits can be weighed based on the priorities of the patient. There are many different methods of crown fabrication, each using a different material. Some methods are quite similar, and utilize either very similar or identical materials. Full gold crowns (FGCs) consist entirely of a single piece of alloy. Although referred to as a gold crown, this type of crown is actually composed of many different types of elements, including but not limited to gold, platinum, palladium, silver, copper and tin. The first four elements listed are noble metals, while the last two listed are base metals. Full gold crowns are of better quality when they are high in noble content. According to the American Dental Association, full gold crown alloys can only be labeled as high noble when they contain at least 60% noble metal, of which at least 40% must be gold. The process of constructing a full gold crown begins at the dentist's office. The clinician will begin by preparing the tooth by removing enough tooth tissue to allow for the crown. Once the preparation has been finalized the clinician will take an impression which is basically a mold of the patient's mouth. The impression and patient details are sent to a dental laboratory where the dental technician will flow dental gypsum into the impression to make a dental model. This model is an exact reproduction of the situation in the patient's mouth. The dental technician now has the information required to model a wax pattern of the final restoration allowing for the tooth shape, occlusion and preparation. The wax pattern can be removed from the model and a wax sprue pattern is attached. The pattern is now ready to use in the Lost-wax casting technique. It is invested in a gypsum or phosphate-bonded investment material, allowed to set then put into a furnace where the wax is completely burnt out leaving a hole for the gold to be poured in. Once the crown has cooled, the technician can remove the sprue, fit and polish the crown ready for cementation. The crown is returned to the dentists office where they can remove any temporary crown and cement the finished gold crown. Porcelain-fused-to-metal dental crowns (PFMs) have a metal shell on which is fused a veneer of porcelain in a high heat oven. The metal provides strong compression and tensile strength, and the porcelain gives the crown a white tooth-like appearance, suitable for front teeth restorations. These crowns are often made with a partial veneer that covers only the aspects of the crown that are visible. The remaining surfaces of the crown are bare metal. A variety of metal alloys containing precious metals and base metals can be used. The porcelain can be color matched to the adjacent teeth. Full-implant-restoration The CAD/CAM method of fabricating all-ceramic restorations is by electronically capturing and storing a photographic image of the prepared tooth and, using computer technology, crafting a 3D restoration design that conforms to all the necessary specifications of the proposed inlay, onlay or single-unit crown; there is no impression. After selecting the proper features and making various decisions on the computerized model, the dentist directs the computer to send the information to a local milling machine. This machine will then use its specially designed diamond burs to mill the restoration from a solid ingot of a ceramic of pre-determined shade to match the patient's tooth. After about 20 minutes, the restoration is complete, and the dentist sections it from the remainder of the unmilled ingot and tries it in the mouth. If the restoration fits well, the dentist can cement the restoration immediately. A dental CAD/CAM machine costs roughly $100,000, with continued purchase of ceramic ingots and milling burs. Typically, over 95% of the restorations made using Dental CAD/CAM and Vita Mark I and Mark II blocks are still clinically successful after 5 years. Further, at least 90% of restorations still function successfully after 10 years. Advantages of the Mark II blocks over ceramic blocks include: they wear down as fast as natural teeth, their failure loads are very similar to those of natural teeth, and the wear pattern of Mark II against enamel is similar to that of enamel against enamel. Popularly known as the "Empress Crown," the leucite reinforced system is superficially similar to a gold crown technique in that a hollow investment pattern is made, but the similarities stop there. A specially designed pressure-injected -reinforced ceramic is then pressed into the mold by using a pressable-porcelain-oven, as though the final all-ceramic restoration has been "cast." The crown that is constructed can be stained and glazed or cut-back and layered with feldspathic ceramic to match the patients natural color and shape. A study by the Umeå University in Sweden, led by Göran Sjögren, sought to study the effectiveness of leucite-reinforced crowns. Titled “Clinical examination of leucite-reinforced glass ceramic crowns (Empress) in general practice: a restrospective study”, it found Empress crowns cracked at approximately only a 6% rate, with the integrity of 86% of the remaining samples being called "excellent." Alumina was introduced as a dental substructure (core) in 1989 when the material was slip cast, sintered, and infiltrated with glass. More recently, glass-infiltrated alumina cores are produced by electrophoretic deposition, a rapid nanofabricating process. During this process particles of a slip are brought to the surface of a dental die by an electric current, thereby forming a precision-fitting core greenbody in seconds. Margins are then trimed and the greenbody is sintered and infiltrated with glass. Glass-infiltrated alumina has significantly higher porcelain bond strength over CAD/CAM produced zirconia and alumina cores without glass. Alumina cores without glass are produced by milling pre-sintered blocks of the material utilizing a CAD/CAM dentistry technique. Cores without glass must be oversized to compensate for shrinkage that occures when the core is fully sintered. Milled cores are then sintered and shrink to the correct size. All alumina cores are layered with aesthetic feldspathic porcelain to make true-to-life color and shape. Dental artists called ceramists, can customize the "look" of these crowns to individual patient and dentist requirements. Today, poreclain fused to alumina crowns set the standard for high aesthetics in dentistry. Zirconia is a very hard ceramic that is used as a strong base material in some full ceramic restorations. The zirconia used in dentistry is zirconium oxide which has been stabilized with the addition of yttrium oxide. The full name of zirconia used in dentistry is yttria-stabilized zirconia or YSZ. The zirconia substructure (core) is usually designed on a digital representation of the patients mouth, which is captured with a 3d digital scan of the patient, impression, or model. The core is then milled from a block of zirconia in a soft pre-sintered state. Once milled, the pre-sintered zirconia is sintered in a furnace where it shrinks by 20% and reaches its full strength of approximately 850MPa. The zirconia core structure can be layered with aesthetic feldspathic porcelain to create the final color and shape of the tooth. Because bond strength of layered porcelain fused to zirconia is not strong, "monolithic" zirconia crowns are often made entirely of the zirconia ceramic with no aesthetic porcelain layered on top. Zirconia is the hardest known ceramic in industry and the strongest material used in dentistry. Monolithic zirconia crowns tend to be dense in appearance with a high value and they lack translucency and fluorescence. For aesthetic reasons, many dentists will not use monolithic crowns on anterior (front) teeth: "Where and When Is It Appropriate to Place Monolithic vs. Layered Restorations," Inside Dentistry, August 2012, Vol. 8, Issue 8, E. McLaren, R. Margeas, N. Fahl. By using crowns made of metal zirconia, then merge the porcelain on the outside, zirconia crowns allow light to pass as a normal tooth would and that gives a natural look, unlike other metal cores that are block the light. The normal too hot/cold sensations you can feel with other crowns does not normally occur because of the lack of electrical conductivity, this being another strong point for zirconia. Dental restoration: Bridge (Resin retained bridge, Rochette bridge)  Crown (Post and core)  Inlays and onlays  Veneer
M: TTH anat/devp/phys noco/cong/jaws/tumr, epon, injr dent, proc (endo, orth, pros)
Bruxism refers to excessive grinding of the teeth and/or excessive clenching of the jaw. Bruxism is an oral parafunctional activity; i.e., not an activity related to normal function such as eating or talking. Bruxism is a common problem: reports of prevalence range from 8–31% in the general population. Even elevated levels of bruxism may cause minimal symptoms, and therefore a bruxer may not be aware of the condition. Several symptoms are commonly associated with bruxism, including hypersensitive teeth, aching jaw muscles, and headaches. Bruxism may cause tooth wear, and may even cause teeth to break and dental restorations (e.g. crowns and fillings) to be repeatedly lost or damaged. There are two main types of bruxism: that which occurs during sleep (sleep bruxism) and that which occurs during wakefulness (awake bruxism). Damage to the teeth may be similar in both types, but the symptoms of sleep bruxism are usually worst upon waking and improve during the course of the day, and the symptoms of awake bruxism may not be present at all upon waking, and then worsen over the day. The causes of bruxism are not completely understood, but probably involve multiple factors. Awake bruxism is thought to have different causes to sleep bruxism, and is more common in females whereas males and females are affected in equal proportions by sleep bruxism. Several treatments are in use, although there is little evidence of robust efficacy for any particular treatment. Bruxism is derived from the Greek word βρυγμός (brygmós), meaning "gnashing of teeth". People who suffer with bruxism may also be called "bruxists", and the act itself "to brux". There is no widely accepted definition of bruxism, but some suggested definitions include: "A movement disorder of the masticatory system charactized by teeth grinding and clenching during sleep as well as wakefulness." "Non-functional contact of the mandibular and maxillary teeth resulting in clenching or tooth grinding due to repetitive, unconscious contraction of the masseter and temporalis muscles." "Parafunctional grinding of teeth or an oral habit consisting of involuntary rhythmic or spasmodic non-functional gnashing, grinding or clenching of teeth in other than chewing movements of the mandible which may lead to occlusal trauma." "Periodic repetitive clenching or rhythmic forceful grinding of the teeth." Bruxism can be subdivided into two types based upon when the parafunctional activity occurs – during sleep ("sleep bruxism"), or whilst awake ("awake bruxism"). This distinction is most widely referred to since sleep bruxism generally has different causes to awake bruxism, although the affects of condition on the teeth may be the same. The treatment is also often dependent upon whether the bruxism happens during sleep or whilst awake. E.g., an occlusal splint worn during sleep in a person who only bruxes when they are awake will probably have no benefit. Some have even suggested that sleep bruxism is an entirely different disorder and is not associated with awake bruxism. Awake bruxism is sometimes abbreviated to AB, and is also termed "diurnal bruxism", DB, or "daytime bruxing". Sleep bruxism is sometimes abbreviated to SB, and is also termed "sleep-related bruxism", "nocturnal bruxism", or "nocturnal tooth grinding". According to the International Classification of Sleep Disorders revised edition (ICSD-R), the term "sleep bruxism" is the most appropriate since this type occurs during sleep specifically rather than being associated with a particular time of day, i.e. if a person with sleep bruxism were to sleep during the day and stay awake at night then the condition would not occur during the night but during the day. The ICDS-R defined sleep bruxism as "a stereotyped movement disorder characterized by grinding or clenching of the teeth during sleep", classifying it as a parasomnia. The second edition (ICSD-2) however reclassified bruxism to a "sleep related movement disorder" rather than a parasomnia. Alternatively, bruxism can be divided into primary bruxism (also termed "idiopathic bruxism"), where the disorder is not related to any other medical condition, or secondary bruxism where the disorder is associated with other medical conditions. Secondary bruxism includes iatrogenic causes, such as the side effect of prescribed medications. Another source divides the causes of bruxism into 3 groups, namely central or pathophysiological factors, psychosocial factors and peripheral factors. The World Health Organization's International Classification of Diseases 10th revision does not have an entry called bruxism, instead listing "tooth grinding" under somatoform disorders. To describe bruxism as a purely somatoform disorder does not reflect the mainstream, modern view of this condition (see causes). The ICSD-R described three different severities of sleep bruxism, defining mild as occurring less than nightly, with no damage to teeth or psychosocial impairment; moderate as occurring nightly, with mild impairment of psychosocial functioning; and severe as occurring nightly, and with damage to the teeth, tempormandibular disorders and other physical injuries, and severe psychosocial impairment. The ICSD-R also described three different types of sleep bruxism according to the duration the condition is present, namely acute, which lasts for less than 1 week; subacute, which lasts for more than a week and less than a month; and chronic which lasts for over a month. Most people who brux are unaware of the problem, either because there are no symptoms, or because the symptoms are not understood to be associated with a clenching and grinding problem. The symptoms of sleep bruxism are usually most intense immediately after waking, and then slowly get better, and the symptoms of a bruxing habit which occurs mainly while awake tend to slowly get worse throughout the day, and may not be present upon waking. Bruxism may cause a variety of signs and symptoms, including: The muscles of mastication (the temporalis, masseter, medial and lateral pterygoid muscles) are paired on either side and work together to move the mandible, which hinges and slides around its dual articulation with the skull at the temporomandibular joints. Some of the muscles work to elevate the mandible (close the mouth), and others also are involved in lateral (side to side), protrusive or retractive movements. Mastication (chewing) is a complex neuromuscular activity that can be controlled either by subconscious processes or by conscious processes. In individuals without bruxism or other parafunctional activities, during wakefulness the jaw is generally at rest and the teeth are not in contact, except whilst speaking, swallowing or chewing. It is estimated that the teeth are in contact for less than 20 minutes per day, mostly during chewing and swallowing. Normally during sleep, the voluntary muscles are inactive due to physiologic motor paralysis, and the jaw is usually open. Some bruxism activity is rhythmic with bite force pulses of tenths of a second (like chewing), and some have longer bite force pulses of 1 to 30 seconds (clenching). Some individuals clench without significant lateral movements. Bruxism can also be regarded as a disorder of repetitive, unconscious contraction of muscles. This typically involves the masseter muscle and the anterior portion of the temporalis (the large outer muscles that clench), and the lateral pterygoids, relatively small bilateral muscles that act together to perform sideways grinding. The cause of bruxism is largely unknown, but it is generally accepted to have multiple possible causes. Bruxism is a parafunctional activity, but it is debated whether this represents a subconscious habit or is entirely involuntary. The relative importance of the various identified possible causative factors are also debated. Awake bruxism is thought to be usually semivoluntary, and often associated with stress caused by family responsibilities or work pressures. Some suggest that in children, bruxism may occasionally represent a response to earache or teething. Awake bruxism usually involves clenching, (sometimes the term "awake clenching" is used instead of awake bruxism), but also possibly grinding, and is often associated with other semivoluntary oral habits such as cheek biting, nail biting, chewing on a pen or pencil absent mindedly, or tongue thrusting (where the tongue is pushed against the front teeth forcefully). There is evidence that sleep bruxism is caused by mechanisms related to the central nervous system, involving sleep arousal and neurotransmitter abnormalities. Underlying these factors may be psychosocial factors including daytime stress which is disrupting peaceful sleep. Sleep bruxism is mainly characterized by "rhythmic masticatory muscle activity" (RMMA) at a frequency of about once per second, and also with occasional tooth grinding. It has been shown that the majority (86%) of sleep bruxism episodes occur during periods of sleep arousal. One study reported that sleep arousals which were experimentally induced with sensory stimulation in sleeping bruxists triggered episodes of sleep bruxism. Sleep arousals are a sudden change in the depth of the sleep stage, and may also be accompanied by increased heart rate, respiratory changes and muscular activity, such as leg movements. Initial reports have suggested that episodes of sleep bruxism may be accompanied by gastroesophageal reflux, decreased esophageal pH (acidity), swallowing, and decreased salivary flow. Another report suggested a link between episodes of sleep bruxism and a supine sleeping position (lying face up). Disturbance of the dopaminergic system in the central nervous system has also been suggested to be involved in the etiology of bruxism. Evidence for this comes from observations of the modifying effect of medications which alter dopamine release on bruxing activity, such as levodopa, amphetamines or nicotine. Nicotine stimulates release of dopamine, which is postulated to explain why bruxism is twice as common in smokers compared to non-smokers. Many studies have reported significant psychosocial risk factors for bruxism, particularly a stressful lifestyle, and this evidence is growing, but still not conclusive. Some consider emotional stress to be the main triggering factor. It has been reported that persons with bruxism respond differently to depression, hostility and stress compared to people without bruxism. Stress has a stronger relationship to awake bruxism, but the role of stress in sleep bruxism is less clear, with some stating that there is no evidence for a relationship with sleep bruxism. However, children with sleep bruxism have been shown to have greater levels of anxiety than other children. People aged 50 with bruxism are more likely to be single and have a high level of education. Work related stress and irregular work shifts may also be involved. Personality traits are also commonly discussed in publications concerning the causes of bruxism, e.g. aggressive, competitive or hyperactive personality types. Some suggest that suppressed anger or frustration can be contribute to bruxism. Stressful periods such as examinations, family bereavement, marriage or moving house have been suggested to intensify bruxism. Awake bruxism often occurs during periods of concentration such as while working at a computer, driving or reading. Animal studies have also suggested a link between bruxism and psychosocial factors. Rosales et al. electrocuted lab rats, and then observed high levels of bruxism-like muscular activity in rats that were allowed to watch this treatment compared to rats that did not see it. They proposed that the rats who witnessed the electrocution of other rats were under emotional stress which may have caused the bruxism-like behavior. Some research suggests that there may be a degree of inherited susceptibility to develop sleep bruxism. 21–50% of people with sleep bruxism have a direct family member who had sleep bruxism during childhood, suggesting that there are genetic factors involved, although no genetic markers have yet been identified. Offspring of people who have sleep bruxism are more likely to also have sleep bruxism than children of people who do not have bruxism, or people with awake bruxism rather than sleep bruxism. Certain drugs, including both prescribed and recreational drugs are thought to cause bruxism to develop, however others argue that there is insufficient evidence to draw conclusion between the effect of any medication and bruxism. Examples include dopamine agonists, dopamine antagonists, tricyclic antidepressants, selective serotonin reuptake inhibitors, alcohol, cocaine, amphetamines (including those taken for medical reasons). In some reported cases when bruxism is thought to have been initiated by selective serotonin reuptake inhibitors, decreasing the dose resolved the side effect, Other sources state that reports of selective serotonin reuptake inhibitors causing bruxism are rare, and only happens with long term use. Specific examples include levodopa (when used in the long term, as in Parkinson's disease), fluoxetine, metoclopramide, lithium, cocaine, venlafaxine, citalopram, fluvoxamine, methylenedioxyamphetamine (MDA), methylphenidate (used in attention deficit hyperactive disorder), and gamma-hydroxybutyric acid (GHB) and similar gamma-aminobutyric acid-inducing analogues such as phenibut. Bruxism can also be exacerbated by excessive consumption of caffeine, such as coffee, tea or chocolate. Bruxism was also reported to occur more commonly in drug addiction. Methylenedioxymethamphetamine (MDMA, ecstasy) has been reported to be associated with bruxism, which occurs immediately after taking the drug and for several days afterwards. Tooth wear in people who take ecstasy is also frequently much more severe than in people with bruxism not associated with ecstasy. Occlusion is defined most simply as "contacts between teeth", and refers to the meeting of teeth during biting and chewing. The term does not imply any disease. Malocclusion is a medical term referring to less than ideal positioning of the upper teeth relative to the lower teeth, which can occur both when the upper jaw is ideally proportioned to the lower jaw, or where there is a discrepancy between the size of the upper jaw relative to the lower jaw. Malocclusion of some sort is so common that the concept of an "ideal occlusion" is called into question, and it can be considered "normal to be abnormal". An an occlusal interference may refer to a problem which interferes with the normal path of the bite, and is usually used to describe a localized problem with the position or shape of a single tooth or group of teeth. A premature contact is a term that refers to one part of the bite meeting sooner than other parts, meaning that the rest of the teeth meet later or are held open. E.g. a new dental restoration on a tooth (e.g. a crown) which has a slightly different shape or position to the original tooth may contact too soon in the bite. A deflective interference refers to an interference with the bite that changes the normal path of the bite. A common example of a deflective is an over-erupted upper wisdom tooth, often because the lower wisdom tooth has been removed. In this example, when the jaws are brought together, the lower back teeth contact the prominent wisdom tooth before the other teeth, and the lower jaw has to move forward to get the rest of the teeth to meet. The difference between a premature contact and a deflective interference is that the latter implies a dynamic abnormality in the bite. Historically, many believed that problems with the bite were the sole cause for bruxism. It was often claimed that a person would grind at the interefering area in a subconscious, instinctive attempt to wear this down and "self equiliberate" their occlusion. However, occlusal interferences are extremely common and usually do not cause any problems. It is unclear whether people with bruxism tend to notice problems with the bite because of their clenching and grinding habit, or whether these act as a causative factor in the development of the condition. In sleep bruxism especially, there is no evidence that removal of occlusal intereferences has any impact on the condition. People with no teeth at all, who wear dentures can still suffer from bruxism, (although dentures too often change the original bite). Most modern sources state that there is no relationship, or at most a minimal relationship, between bruxism and occlusal factors. The findings of one study, which used self reported tooth grinding rather than clinical examination to detect bruxism, suggested that there may be more of a relationship between occlusal factors and bruxism in children. However, the role of occlusal factors in bruxism cannot be completely discounted due to insufficient evidence and problems with the design of studies. A minority of researchers continue to claim that various adjustments to the mechanics of the bite are capable of curing bruxism (see Occlusal adjustments/reorganization). Several associations between bruxism and other conditions, usually neurological or psychiatric disorders, have rarely been reported, with varying degrees of evidence (often in the form of case reports). Examples include: Bruxism is usually detected because of the effects of the process (most commonly tooth wear and pain), rather than the process itself. The large forces that can be generated during bruxism can have detrimental effects on the components of masticatory system, namely the teeth, the periodontium and the articulation of the mandible with the skull (the temporomandibular joints). The muscles of mastication that act to move the jaw can also be affected since they are being utilized over and above of normal function. Many publications list tooth wear as a consequence of bruxism, but some report a lack of a positive relationship between tooth wear and bruxism. Tooth wear caused by tooth to tooth contact is termed attrition. This is the most usual type of tooth wear that occurs in bruxism, and affects the occlusal surface (the biting surface) of the teeth. The exact location and pattern of attrition depends on how the bruxism occurs. E.g. when the canines and incisors of the opposing arches are moved against each other laterally, by the action of the medial pterygoid muscles, this can lead to the wearing down of the incisal edges of the teeth. To grind the front teeth, most people need to posture their mandible forwards, unless there is an existing edge to edge, class III incisal relationship. People with bruxism may also grind their posterior teeth (back teeth), which wears down the cusps of the occlusal surface. Once tooth wear progresses through the enamel layer, the exposed dentin layer is softer and more vulnerable to wear and tooth decay. If enough of the tooth is worn away or decayed, the tooth will effectively be weakened, and may fracture under the increased forces that occur in bruxism. Abfraction is another type of tooth wear that is postulated to occur with bruxism, although some still argue whether this type of tooth wear is a reality. Abfraction cavities are said to occur usually on the facial aspect of teeth, in cervical region as V-shaped defects caused by flexing of the tooth under occlusal forces. It is argued that similar lesions can be caused by long term forceful toothbrushing. However, the fact that the cavities are V-shaped does not suggest that the damage is caused by toothbush abrasion, and that some abfraction cavities occur below the level of the gumline, i.e. in an area shielded from toothbrush abrasion, supports the validity of this mechanism of tooth wear. In addition to attrition, erosion is said to synergistically contribute to tooth wear in some bruxists, according to some sources. The view that occlusal trauma (as may occur during bruxism) is a causative factor in gingivitis and periodontitis is not widely accepted. It is thought that the periodontal ligament may respond to increased occlusal (biting) forces by resorbing some of the bone of the alveolar crest, which may result in increased tooth mobility, however these changes are reversible if the occlusal force is reduced. Tooth movement that occurs during occlusal loading is sometimes termed fremitus. It is generally accepted that increased occlusal forces are able to increase the rate of progression of pre-existing periodontal disease (gum disease), however the main stay treatment is plaque control rather than elaborate occlusal adjustments. It is also generally accepted that periodontal disease is a far more common cause of tooth mobility and pathological tooth migration than any influence of bruxism, although bruxism may much less commonly be involved in both. Most people with bruxism will not experience any pain. Furthermore, the presence or degree of pain does not necessarily correlate with the severity of grinding or clenching that is occurring. The pain in the muscles of mastication caused by bruxism can be likened to muscle pain that occurs after exercise. The pain may be felt over the angle of the jaw (masseter) or in the temple (temporalis), and is may be described as a headache or an aching jaw. Most (but not all) bruxism includes clenching force provided by masseter and temporalis muscle groups; but some bruxers clench and grind front teeth only, which involves minimal action of the masseter and temporalis muscles. The temporomandibular joints themselves may also become painful, which is usually felt just in front of the ear, or inside the ear itself. Clicking of the jaw joint may also develop. The forces exerted on the teeth are more than the periodontal ligament is biologically designed to handle, and so inflammation may result. The tooth may become sore to bite on, and further, tooth wear may reduce the insulating width of enamel and dentin that protects the pulp of the tooth and result in hypersensitivity, e.g. to cold stimuli. The relationship of bruxism with temporomandibular joint dysfunction (TMD, or temporomandibular pain dysfunction syndrome) is debated. Many suggest that sleep bruxism can be a causative or contributory factor to pain symptoms in TMD. Indeed, the symptoms of TMD overlap with those of bruxism. Others suggest that there is no strong association between TMD and bruxism. A systematic review investigating the possible relationship concluded that when self reported bruxism is used to diagnose bruxism, there is a positive association with TMD pain, and when more strict diagnostic criteria for bruxism are used, the association with TMD symptoms is much lower. In severe, chronic cases, bruxism can lead to myofascial pain and arthritis of the temporomandibular joints.][ Early diagnosis of bruxism is advantageous, due to the possible damage that may be incurred and the detrimental effect on quality of life. A diagnosis of bruxism is usually made clinically, and is mainly based on the person's history (e.g. reports of grinding noises) and the presence of typical signs and symptoms, including tooth mobility, tooth wear, masseteric hypertrophy, indentations on the tongue, hypersensitive teeth (which may be misdiagnosed as reversible pulpitis), pain in the muscles of mastication, and clicking or locking of the temporomandibular joints. Questionnaires can be used to screen for bruxism in both the clinical and research settings. The Individual (personal) Tooth-Wear Index was developed to objectively quantify the degree of tooth wear in an individual, without being affected by the number of missing teeth. Bruxism is not the only cause of tooth wear. Another possible cause of tooth wear is acid erosion, which may occur in people who drink a lot of acidic liquids such as concentrated fruit juice, or in people who frequently vomit or regurgitate stomach acid, which itself can occur for various reasons. People also demonstrate a normal level of tooth wear, associated with normal function. The presence of tooth wear only indicates that it has occurred at some point in the past, and does not necessarily indicate that the loss of tooth substance is ongoing. People who clench and perform minimal grinding will also not show much tooth wear. Occlusal splints are usually employed as a treatment for bruxism, but they can also be of diagnostic use, e.g. to observe the presence or absence of wear on the splint after a certain period of wearing it at night. The most usual trigger in sleep bruxism that leads a person to seek medical or dental advice is being informed by sleeping partner of unpleasant grinding noises during sleep. The diagnosis of sleep bruxism is usually straightforward, and involves the exclusion of dental diseases, temporomandibular disorders, and the rhythmic jaw movements that occur with seizure disorders (e.g. epilepsy). This usually involves a dental examination, and possibly electroencephalography if a seizure disorder is suspected. Polysomnography shows increased masseter and temporalis muscular activity during sleep. Polysomnography may involve electroencephalography, electromyography, electrocardiography, air flow monitoring and audio–video recording. It may be useful to help exclude other sleep disorders, however due to the expense of the use of a sleep lab, polysomnography is mostly of relevance to research rather than routine clinical diagnosis of bruxism. Tooth wear may be brought to the person's attention during routine dental examination. With awake bruxism, most people will often initially deny clenching and grinding because they are unaware of the habit. Often, the person may re-attend soon after the first visit and report that they have now become aware of such a habit. Several devices have been developed that aim to objectively measure bruxism activity, either in terms of muscular activity or bite forces. They have been criticized for introducing a possible change in the bruxing habit, whether increasing or decreasing it, and are therefore poorly representative to the native bruxing activity. These are mostly of relevance to research, and are rarely used in the routine clinical diagnosis of bruxism. Examples include the "Bruxcore Bruxism-Monitoring Device" (BBMD, "Bruxcore Plate"), the "intra-splint force detector" (ISFD), and electromyographic devices to measure masseter or temporalis muscle activity (e.g. the "BiteStrip", and the "Grindcare"). The ICSD-R listed diagnostic criteria for sleep bruxism. The minimal criteria include both of the following: With the following criteria supporting the diagnosis: Treatment for bruxism revolves around repairing the damage to teeth that has already occurred, and also often, via one or more of several available methods, attempting to prevent further damage and manage symptoms, but there is no widely accepted, best treatment. Since bruxism is not life threatening, and there is little evidence of the efficacy of any treatment, it has been recommended that only conservative treatment which is reversible and that carries low risk of morbidity should be used. The main treatments that have been described in awake and sleep bruxism are described below, and others include physiotherapy Bruxism can cause significant tooth wear if it is severe, and sometimes dental restorations (crowns, fillings etc.) are damaged or lost, sometimes repeatedly. Most dentists therefore prefer to keep dental treatment in people with bruxism very simple and only carry it out when essential, since any dental work is likely to fail in the long term. Dental implants and complex bridgework for example are relatively contraindicated in bruxists. In the case of crowns, the strength of the restoration becomes more important, sometimes at the cost of esthetic considerations. E.g. a full coverage gold crown, which has a degree of flexibility and also involves less removal (and therefore less weakening) of the underlying natural tooth may be more appropriate than other types of crown which are primarily designed for esthetics rather than durability. Porcelain veneers on the incisors are particularly vulnerable to damage, and sometimes a crown can be perforated by occlusal wear. Occlusal splints (also termed dental guards) are commonly prescribed, mainly by dentists, as a treatment for bruxism. Proponents of their use claim many benefits, however when the evidence is critically examined in systematic reviews of the topic, it is reported that there is insufficient evidence to show that occlusal splints are effective for sleep bruxism. Occlusal splints probably are ineffective for awake bruxism, since they are usually worn during sleep only. However, occlusal splints may be of some benefit in reducing the tooth wear that may accompany bruxism. Occlusal splints are divided into partial or full-coverage splints according to whether they fit over some or all of the teeth. They are typically made of plastic (e.g. acrylic][) and can be hard or soft. A lower appliance can be worn alone, or in combination with an upper appliance. Usually lower splints are better tolerated in people with a sensitive gag reflex. Another problem with wearing a splint can be stimulation of salivary flow, and for this reason some advise to start wearing the splint about 30 mins before going to bed so this does not lead to difficulty falling asleep. As an added measure for hypersensitive teeth in bruxism, desensitizing tooth pastes (e.g. containing strontium chloride) can be applied initially inside the splint so the material is in contact with the teeth all night. This can be continued until there is only a normal level of sensitivity from the teeth, although it should be remembered that sensitivity to thermal stimuli is also a symptom of pulpitis, and may indicate the presence of tooth decay rather than merely hypersensitve teeth. Splints may also reduce muscle strain by allowing the upper and lower jaw to move easily with respect to each other. Treatment goals include: constraining the bruxing pattern to avoid damage to the temporomandibular joints; stabilizing the occlusion by minimizing gradual changes to the positions of the teeth, preventing tooth damage and revealing the extent and patterns of bruxism through examination of the markings on the splint's surface. A dental guard is typically worn during every night's sleep on a long-term basis. However, a meta-analysis of occlusal splints (dental guards) used for this purpose concluded "There is not enough evidence to state that the occlusal splint is effective for treating sleep bruxism." A repositioning splint is designed to change the patient's occlusion, or bite.][ The efficacy of such devices is debated. Some writers propose that irreversible complications can result from the long-term use of mouthguards and repositioning splints. Random controlled trials with these type devices generally show no benefit over other therapies. Another partial splint is the "nociceptive trigeminal inhibitor tension suppression system" (NTI-TSS) dental guard. This splint snaps onto the upper front teeth only. It is theorized to prevent tissue damages primarily by reducing the bite force from attempts to close the jaw normally into a forward twisting of the lower front teeth. The intent is for the brain to interpret the nerve sensations as undesirable, automatically and subconsciously reducing clenching force. However there may be potential for the NTI-TSS device to act as a Dahl appliance, holding the posterior teeth out of occlusion and leading to their over-eruption, deranging the occlusion. Hence, ongoing follow-ups are recommended. In a minority of cases, sleep bruxism may be made worse by an occlusal splint. A mandibular advancement device (normally used for treatment of obstructive sleep apnea) may reduce sleep bruxism, although its use may be associated with discomfort. Given the strong association between awake bruxism and psychosocial factors (the relationship between sleep bruxism and psychosocial factors being unclear), the role of psychosocial interventions could be argued to be central to the management. The most simple form of treatment is therefore reassurance that the condition does not represent a serious disease, which may act to alleviate contributing stress. Other interventions include relaxation techniques, stress management, behavioural modification, habit reversal and hypnosis (self hypnosis or with a hypnotherapist). Cognitive behavioral therapy has been recommended by some for treatment of bruxism. Many different medications have been used to treat bruxism, including benzodiazepines, anticonvulsants, beta blockers, dopamine agents, antidepressants, muscle relaxants, and others. However there is little, if any, evidence for their respective and comparative efficacies with each other and when compared to a placebo. A systematic review is underway to investigate the evidence for drug treatments in sleep bruxism. Specific drugs which have been studied in sleep bruxism include pergolide, clonidine, propranolol, and l-tryptophan, with some showing no effect and others appear to have promising initial results, however it has been suggested that further safety testing is required before any evidenced based clinical recommendations can be made. When bruxism is related to the use of selective serotonin reuptake inhibitors in depression, adding buspirone has been reported to resolve the side effect. Tricyclic antidepressants have also been been suggested to be preferable to selective serotinin reuptake inhibitors in people with bruxism, and may help with the pain. Botulinum toxin (Botox) has been suggested as a treatment for bruxism, however there is only one randomized control trial which has reported that Botox reduces the myofascial pain symptoms. This scientific study was based on thirty people with bruxism who received Botox injections into the muscles of mastication and a control group of people with bruxism who received placebo injections. Normally multiple trials with larger cohorts are required to make any firm statement about the efficacy of a treatment. In 2013, a further randomized control trial investigating Botox in bruxism started. There is also little information available about the safety and long term follow up of this treatment for bruxism. Botulinum toxin causes muscle paralysis by inhibition of acetylcholine release at neuromuscular junctions. Botox injections are used in bruxism on the theory that a dilute solution of the toxin will partially paralyze the muscles and lessen their ability to forcefully clench and grind the jaw, whilst aiming to retain enough muscular function to enable normal activities such as talking and eating. This treatment typically involves five or six injections into the masseter and termporalis muscles, and less often into the lateral pterygoids, (given the possible risk of decreasing the ability to swallow). It takes a few minutes per side, and the patient may start feeling the effects by the next day, and may last for about three months. Occasionally, adverse effects may occur, such as bruising can occur, but this is quite rare. The dose of toxin used depends upon the person, and a higher dose may be needed in people with stronger muscles of mastication. With the temporary and partial muscle paralysis, atrophy of disuse may occur, meaning that the future required dose may be smaller or the length of time the effects last may be increased. Biofeedback refers to a process (or device that enables such a process) that allows an individual to become aware of, and alter physiolgoical actvity with the aim of improving health. There is no evidence for the long term use and safety of biofeedback in the management of bruxism. Electromyographic monitoring of the muscles with automatic alerting during periods of clenching and grinding has been described for awake bruxism. Dental appliances with capsules that break and release a taste stimulus when enough force is applied have also been described in sleep bruxism, which would wake the person from sleep in an attempt to prevent bruxism episodes. Unfortunately this resulted in excessive daytime sleepiness. An alternative to simply re-actively repairing the damage to teeth and conforming to the existing occlusal scheme, occasionally some dentists will attempt to reorganize the occlusion in the belief that this may redistribute the forces and reduce the amount of damage inflicted on the dentition. Sometimes termed "occlusal rehabilitation" or "occlusal equilibration", this can be a complex procedure, and there is much disagreement between proponents of these techniques on most of the aspects involved, including the indications and the goals. It may involve orthodontics, restorative dentistry or even orthognathic surgery. Some have criticized these occlusal reorganizations as having no evidence base, and irreversibly damaging the dentition on top of the damage already caused by bruxism. There is a wide variation in reported epidemiologic data for bruxism, and this is largely due to differences in the definition, diagnosis and research methodologies of these studies. E.g. several studies use self reported bruxism as a measure of bruxism, and since many people with bruxism are not aware of their habit, self reported tooth grinding and clenching habits may be a poor measure of the true prevalence. The ICSD-R states that 85–90% of the general population grind their teeth to a degree at some point during their life, although only 5% will develop a clinical condition. Some studies have reported that awake bruxism affects females more commonly than males, whilst in sleep bruxism, males are as equally affected as females. Children are reported to brux as commonly as adults. It is possible for sleep bruxism to occur as early as the first year of life – after the first teeth (deciduous incisors) erupt into the mouth, and the overall prevalence in children is about 14–20%. The ICSD-R states that sleep bruxism may occur in over 50% of normal infants. Often sleep bruxism develops during adolescence, and the prevalence in 18 to 29-year olds is about 13%. The overall prevalence in adults is reported to be 8%, and people aver the age of 60 are less likely to be affected, with the prevalence dropping to about 3% in this group. A 2013 systematic review of the epidemiologic reports of bruxism concluded a prevalence of about 22.1–31% for awake bruxism, 9.7–15.9% for sleep bruxism, and an overall prevalence of about 8–31.4% of bruxism generally. The review concluded that overall, bruxism affects males and females equally, and affects elderly people less commonly. "La bruxomanie" (a French term roughly equivalent to bruxomania), is suggested by Marie Pietkiewics in 1907. In 1931, Frohman first coined the term bruxism. Occasionally recent medical publications will use the word bruxomania with bruxism, to denote specifically bruxism that occurs whilst awake, however this term can be considered historical and the modern equivalent would be awake bruxism or diurnal bruxism. It has been shown that the type of research into bruxism has changed over time. Overall between 1966 and 2007, most of the research published was focused on occlusal adjustments and oral splints. Behavioral approaches in research declined from over 60% of publications in the period 1966–1986 to about 10% in the period 1997–2007. Ramjford championed the theory that occlusal factors were responsible for bruxism in the 1960s, however the vast majority of researchers now disfavor this theory. Clenching the teeth is generally displayed by humans and other animals as a display of anger, hostility or frustration. It is thought that in humans, clenching the teeth may be an evolutionary instinct to display teeth as weapons, thereby threaten a rival or a predator. The phrase "to grit one's teeth" refers to grinding or clenching of the teeth in anger, or to accept a difficult or unpleasant situation and deal with it in a determined way. In the Bible there are several references to "gnashing of teeth" in both the Old Testament, and the New Testament particularly, where the phrase "wailing and gnashing of teeth" is used to described the fate of sinners in hell (). In the 2005 film Beowulf & Grendel, a modern reworking of the Anglo-Saxon poem Beowulf, Selma the witch tells Beowulf that the troll's name Grendel means "grinder of teeth", stating that "he has bad dreams", a possible allusion to Grendel traumatically witnessing the death of his father as a child, at the hands of King Hrothgar. The Geats (the warriors who hunt the troll) alternatively translate the name as "grinder of mens' bones" to demonize their prey. In rave culture, recreational use of ecstasy causes many health problems, and bruxism is often reported by users. Whilst dancing, it is common to use pacifiers, lollipops or chewing gum in an attempt to reduce the damage to the teeth and to prevent jaw pain. M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D) M: CNS anat (n/s/m/p/4/e/b/d/c/a/f/l/g)/phys/devp noco (m/d/e/h/v/s)/cong/tumr, sysi/epon, injr proc, drug (N1A/2AB/C/3/4/7A/B/C/D) M: PSO/PSI mepr dsrd (o, p, m, p, a, d, s), sysi/epon, spvo proc (eval/thrp), drug (N5A/5B/5C/6A/6B/6D)
Tooth loss is a process in which one or more teeth come loose and fall out. Tooth loss is normal for deciduous teeth (baby teeth), when they are replaced by a person's adult teeth. Otherwise, losing teeth is undesirable and is the result of injury or disease, such as mouth trauma, tooth injury, tooth decay, and gum disease. The condition of being toothless or missing one or more teeth is called edentulism. Tooth loss due to tooth decay and gum disease may be prevented by practicing good oral hygiene, and regular check-ups at a dentist's office. In contact sports, risk of mouth trauma and tooth injury is reduced by wearing mouthguards and helmets with a facemask (e.g., a football helmet, a goalie mask). There are three basic ways to replace a missing tooth or teeth, including a fixed dental bridge, dentures, and dental implants. Researchers in Japan have successfully regrown fully functional teeth in mice. Epithelial and mesenchymal cells were extracted from the mice, cultured to produce a tooth "germ", and the germ was then implanted into the bone at the space of a missing tooth. A tooth of the correct external and internal structure, hardness, strength, and sensitivity later erupted in the space, eventually meeting the opposing tooth in a manner similar to an original natural tooth. This technique may be a possible future treatment for replacement of missing teeth.
Vertical root fractures are a type of fracture of a tooth. They can be characterized by an incomplete or complete fracture line that extends through the long axis of the root toward the apex. Vertical root fractures are between 2 and 5 percent of crown/root fractures. The greatest incidence occurs in endodontically treated teeth and in patients older than 40 years of age. The occurrence of a complete vertical root fracture is often catastrophic for the individual tooth as tooth extraction is usually the only reasonable treatment. Vertical root fracture is more likely where teeth have undergone extensive prior treatment. It is thought that excessive removal of dentine during procedures such as root canal treatment weakens the tooth. For this reason excessive canal shaping is to be avoided. Fracturing may be caused by excessive forces placed on the tooth, such as during compaction of gutta-percha during the obturation phase of endodontics. Trauma can also cause crack formation. Symptoms include: Short duration pain on biting, sensitivity to temperature change. Fracture lines may be visibly evident. Transillumination may reveal unseen fractures. Radiographic changes such as radiolucencies in the region of the fracture may be seen. Vertical root fracture can be a difficult diagnosis to make where the fracture line is not evident. Use of cone-beam computerized tomography has been described. JADA * [1] M: BON/CAR anat (c/f/k/f, u, t/p, l)/phys/devp/cell noco/cong/tumr, sysi/epon, injr proc, drug (M5) M: TTH anat/devp/phys noco/cong/jaws/tumr, epon, injr dent, proc (endo, orth, pros) M: TTH anat/devp/phys noco/cong/jaws/tumr, epon, injr dent, proc (endo, orth, pros)
dentist Crown Tooth Endodontics

Dental bleaching, also known as tooth whitening, is a common procedure in general dentistry. According to the FDA, whitening restores natural tooth color and bleaching whitens beyond the natural color. There are many methods available, such as brushing, bleaching strips, bleaching pen, bleaching gel, and laser bleaching. Teeth whitening has become the most requested procedure in cosmetic dentistry today. More than 100 million Americans whiten their teeth one way or another; spending an estimated $15 billion in 2010.

Bleaching methods use carbamide peroxide which reacts with water to form hydrogen peroxide. Carbamide peroxide has about a third of the strength of hydrogen peroxide. This means that a 15% solution of carbamide peroxide is the rough equivalent of a 5% solution of hydrogen peroxide. The peroxide oxidizing agent penetrates the porosities in the rod-like crystal structure of enamel and breaks down stain deposits in the dentin. Power bleaching uses light to accelerate the process of bleaching in a dental office. Another bleaching agent is 6-phthalimido peroxy hexanoic acid (PAP).

Dentistry Prosthodontology

Restorative dentistry is the study, diagnosis and integrated management of diseases of the teeth and their supporting structures and the rehabilitation of the dentition to functional and aesthetic requirements of the individual. Restorative dentistry encompasses the dental specialties of endodontics, periodontics and prosthodontics and its foundation is based upon how these interact in cases requiring multifaceted care. In the UK restorative dentistry is legally recognized as a specialty under EU directive, with voices from the British Society for Restorative Dentistry and the Association of Consultants & Specialists in Restorative Dentistry.


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Human interest stories may be "the story behind the story" about an event, organization, or otherwise faceless historical happening, such as about the life of an individual soldier during wartime, an interview with a survivor of a natural disaster, a random act of kindness or profile of someone known for a career achievement.

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