The first three cases of bisphosphonate-associated osteonecrosis of the jaw were spontaneously reported to the FDA by an oral surgeon in 2002, with the toxicity being described as a potentially late toxicity of chemotherapy. In 2003 and 2004, three oral surgeons independently reported to the FDA information on 104 cancer patients with bisphosphonate-associated osteonecrosis of the jaw seen in their referral practices in California, Florida, and New York. These case series were published as peer-reviewed articles — two in the "Journal of Oral and Maxillofacial Surgery" and one in the "Journal of Clinical Oncology". Subsequently, numerous instances of persons with this ADR were reported to the manufacturers and to the FDA. By December 2006, 3607 cases of people with this ADR had been reported to the FDA and 2227 cases had been reported to the manufacturer of intravenous bisphosphonates.

The International Myeloma Foundation's web-based survey included 1203 respondents, 904 patients with myeloma and 299 with breast cancer and an estimate that after 36 months, osteonecrosis of the jaw had been diagnosed in 10% of 211 patients on zoledronate and 4% of 413 on pamidronate. A population based study in Germany identified more than 300 cases of osteonecrosis of the jaw, 97% occurring in cancer patients (on high-dose intravenous bisphosphonates) and 3 cases in 780,000 patients with osteoporosis for an incidence of 0.00038%. Time to event ranged from 23–39 months and 42–46 months with high dose intravenous and oral bisphosphonates. A prospective, population based study by Mavrokokki "et al.". estimated an incidence of osteonecrosis of the jaw of 1.15% for intravenous bisphosphonates and 0.04% for oral bisphosphonates. Most cases (73%) were precipitated by dental extractions. In contrast, safety studies sponsored by the manufacturer reported bisphosphonate-associated osteonecrosis of the jaw rates that were much lower.

Although the majority of cases of ONJ have occurred in cancer patients receiving high dose intravenous bisphosphonates, almost 800 cases have been reported in oral bisphosphonate users for osteoporosis or Pagets disease. In terms of severity most cases of ONJ in oral bisphosphonate users are stage 1–2 and tend to progress to resolution with conservative measures such as oral chlorhexidine rinses.

Owing to prolonged embedding of bisphosphonate drugs in the bone tissues, the risk for BRONJ is high even after stopping the administration of the medication for several years.

This form of therapy has been shown to prevent loss of bone mineral density (BMD) as a result of a reduction in bone turnover. However, bone health entails quite a bit more than just BMD. There are many other factors to consider.

In healthy bone tissue there is a homeostasis between bone resorption and bone apposition. Diseased or damaged bone is resorbed through the osteoclasts mediated process while osteoblasts form new bone to replace it, thus maintaining healthy bone density. This process is commonly called remodelling.

However, osteoporosis is essentially the result of a lack of new bone formation in combination with bone resorption in reactive hyperemia, related to various causes and contributing factors, and bisphosphonates do not address these factors at all.

In 2011, a proposal incorporating both the reduced bone turnover and the infectious elements of previous theories has been put forward. It cites the impaired functionality of affected macrophages as the dominant factor in the development of ONJ.

In a systematic review of cases of bisphosphonate-associated ONJ up to 2006, it was concluded that the mandible is more commonly affected than the maxilla (2:1 ratio), and 60% of cases are preceded by a dental surgical procedure. According to Woo, Hellstein and Kalmar, oversuppression of bone turnover is probably the primary mechanism for the development of this form of ONJ, although there may be contributing co-morbid factors (as discussed elsewhere in this article). It is recommended that all sites of potential jaw infection should be eliminated before bisphosphonate therapy is initiated in these patients to reduce the necessity of subsequent dentoalveolar surgery. The degree of risk for osteonecrosis in patients taking oral bisphosphonates, such as alendronate (Fosamax), for osteoporosis is uncertain and warrants careful monitoring. Patients taking dexamethasone and other glucocorticoids are at increased risk.

Matrix metalloproteinase 2 may be a candidate gene for bisphosphonate-associated osteonecrosis of the jaw, since it is the only gene known to be associated with bone abnormalities and atrial fibrillation, both of which are side effects of bisphosphonates.

Other factors such as toxicants can adversely impact bone cells. Infections, chronic or acute, can affect blood flow by inducing platelet activation and aggregation, contributing to a localized state of excess coagulability (hypercoagulability) that may contribute to clot formation (thrombosis), a known cause of bone infarct and ischaemia. Exogenous estrogens, also called hormonal disruptors, have been linked with an increased tendency to clot (thrombophilia) and impaired bone healing.

Heavy metals such as lead and cadmium have been implicated in osteoporosis. Cadmium and lead promotes the synthesis of plasminogen activator inhibitor-1 (PAI-1) which is the major inhibitor of fibrinolysis (the mechanism by which the body breaks down clots) and shown to be a cause of hypofibrinolysis. Persistent blood clots can lead to congestive blood flow (hyperemia) in bone marrow, impaired blood flow and ischaemia in bone tissue resulting in lack of oxygen (hypoxia), bone cell damage and eventual cell death (apoptosis). Of significance is the fact that the average concentration of cadmium in human bones in the 20th century has increased to about 10 times above the pre-industrial level.

Bone erosion is the loss of bone from disease processes like rheumatoid arthritis. Bone erosion is the loss of bone in a certain area, rather than a change in bone density, which is found in osteoporosis. Surprisingly, bone erosion is not found in osteoarthritis.

Paget's disease may be caused by a slow virus infection (i.e., paramyxoviridae) present for many years before symptoms appear. Associated viral infections include respiratory syncytial virus, canine distemper virus, and the measles virus. However, recent evidence has cast some doubt upon the measles association. Laboratory contamination may have played a role in past studies linking paramyxovirus (e.g. measles) to Paget's disease.

Eburnation describes a degenerative process of bone commonly found in patients with osteoarthritis or non-union of fractures. It is an ivory-like reaction of bone occurring at the site of cartilage erosion. Osteoarthritis is a degenerative disease of the joints characterized largely by central loss of cartilage and compensatory peripheral bone formation (osteophytes). Over time, as the cartilage wears away, bare, subchondral bone is revealed. Eburnation describes the bony sclerosis which occurs at the areas of cartilage loss.

The disease is progressive and slowly worsens with time, although people may remain minimally symptomatic. Treatment is aimed at controlling symptoms, but there is no cure. Any bone or bones can be affected, but Paget's disease occurs most frequently in the spine, skull, pelvis, femur, and lower legs.

Osteogenic sarcoma, a form of bone cancer, is a rare complication of Paget's disease occurring in less than one percent of those affected. The development of osteosarcoma may be suggested by the sudden onset or worsening pain.

A bone cyst or geode is a cyst that forms in bone.

Types include:

- Unicameral bone cyst

- Aneurysmal bone cyst

- Traumatic bone cyst

Simple (Unicameral) Bone Cyst

Some unicameral bone cysts may spontaneously resolve without medical intervention. Specific treatments are determined based on size of the cyst, strength of the bone, medical history, extent of the disease, activity level, symptoms an individual is experiencing, and tolerance for specific medications, procedures, or therapies. The types of methods used to treat this type of cyst are curettage and bone grafting, aspiration, steroid injections, and bone marrow injections. Watchful waiting and activity modifications are the most common nonsurgical treatments that will help resolve and help prevent unicameral bone cysts from occurring and reoccurring.

Aneurysmal Bone Cyst

The aneurysmal bone cyst can be treated with a variety of different methods. These methods include open curettage and bone grafting with or without adjuvant therapy, cryotheraphy, sclerotherapy, ethibloc injections, radionuclide ablation, and selective arterial embolization. En-block resection and reconstruction with strut grafting are the most common treatments and procedures that prevent recurrences of this type of cyst.

Traumatic Bone Cyst

The traumatic bone cyst treatment consists of surgical exploration, curettage of the osseous socket and bony walls, subsequent filling with blood, and intralesional steroid injections. Young athletes can reduce their risk of traumatic bone cyst by wearing protective mouth wear or protective head gear.

The exact cause is unknown. Some doctors believe it is caused by abnormal metabolism of fat. Others think it may be caused by repetitive inflammation. Some feel that blood within the joint may cause the inflammatory change. Risk factors for PVNS developing are not yet understood. Very little research has been carried out. However, a common theme in patients is a trauma experienced to the joint prior to the onset of symptoms.

Several risk factors of CMC OA of the thumb are known. Each of these risk factors does not cause CMC OA by itself, but acts as a predisposing factor influencing the process of OA in some way. Risk factors include: female gender, suffering from obesity, repetitive heavy manual labor, familial predisposition and hormonal changes, such as menopause.

CMC OA is the most common form of OA affecting the hand. Dahaghin et al. showed that about 15% of women and 7% of men between 50 and 60 years of age suffer from CMC OA of the thumb. However, in about 65% of people older than 55 years, radiologic evidence of OA was present without any symptoms. Armstrong et al. reported a prevalence of 33% in postmenopausal women, of which one third was symptomatic, compared to 11% in men older than 55 years. This shows CMC OA of the thumb is significantly more prevalent in women, especially in postmenopausal women, compared to men.

Pigmented villonodular synovitis, described distinctly in 1941 by Charles J. Sutro, L. Lichtenstein, and H.L. Jafe, comes in two forms: localized and diffuse. Diffuse PVNS affects the entire synovium and typically occurs in large joints such as the knee or hip. Localized, or nodular, PVNS is less common than the diffuse form and typically occurs in smaller joints such as the hands and feet. Localized PVNS often arises in the form of a large benign tumour on the tendon sheaths of the joint. As the tumor grows in the joint, it damages the surrounding bone and tissues. Localized PVNS is predominantly found in females and is frequently found in the fingers. Although rare, localized PVNS may develop in large joints. In either case, the knee is the most commonly affected joint (80% of cases), followed by the hip, and less commonly the ankles and shoulders. PVNS is generally found more in men than women. 2 cases per million population; incidence of the localized form is 9 cases per million.

A compound elevated skull fracture is a rare type of skull fracture where the fractured bone is elevated above the intact outer table of the skull. This type of skull fracture is always compound in nature. It can be caused during an assault with a weapon where the initial blow penetrates the skull and the underlying meninges and, on withdrawal, the weapon lifts the fractured portion of the skull outward. It can also be caused the skull rotating while being struck in a case of blunt force trauma, the skull rotating while striking an inanimate object as in a fall, or it may occur during transfer of a patient after an initial compound head injury.

Dentinogenesis imperfecta (DI) is a genetic disorder of tooth development. This condition is a type of dentin dysplasia that causes teeth to be discolored (most often a blue-gray or yellow-brown color) and translucent giving teeth an opalescent sheen. Although genetic factors are the main contributor for the disease, any environmental or systemic upset that impedes calcification or metabolisation of calcium can also result in anomalous dentine.

Consequently, teeth are also weaker than normal, making them prone to rapid wear, breakage, and loss. These problems can affect both primary (deciduous) teeth and permanent teeth. This condition is inherited in an autosomal dominant pattern, as a result of mutations on chromosome 4q21, in the dentine sialophosphoprotein gene (DSPP). It is one of the most frequently occurring autosomal dominant feature in humans. Dentinogenesis imperfecta affects an estimated 1 in 6,000 to 8,000 people.

The prognosis for a horse with navicular syndrome is guarded. Many times the horse does not return to its former level of competition. Others are retired. Eventually all horses with the syndrome will need to lessen the strenuousness of their work, but with proper management, a horse with navicular syndrome can remain useful for some time.

A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges—or runs through the paranasal sinuses and the middle ear structures, putting the outside environment in contact with the cranial cavity—is a compound fracture.

Compound fractures may either be clean or contaminated. Intracranial air (pneumocephalus) may occur in compound skull fractures.

The most serious complication of compound skull fractures is infection. Increased risk factors for infection include visible contamination, meningeal tear, loose bone fragments and presenting for treatment more than eight hours after initial injury.

Navicular syndrome, often called navicular disease, is a syndrome of lameness problems in horses. It most commonly describes an inflammation or degeneration of the navicular bone and its surrounding tissues, usually on the front feet. It can lead to significant and even disabling lameness.

Dental attrition is tooth wear caused by tooth to tooth contact. Well-defined wear facets appear on tooth cusps or ridges. This can be caused by several factors, including parafunctional habits such as bruxism or clenching, developmental defects, hard or rough-textured diet, and absence of posterior teeth support. If the natural teeth oppose or occlude with porcelain restorations, then accelerated attrition of the natural teeth may result. Similarly, when an edge to edge class III incisal relationship is present dental attrition can occur. The underlying cause of attrition may be related to the temporomandibular joint as a disruption or dysfunction of the joint can result in compromised function and complications such as bruxism and clenching of the jaw may arise

The etiology of dental attrition is multifactorial one of the most common causes of attrition is bruxism, one of the major causes being the use of MDMA (ecstasy) and various other related entactogenic drugs. Bruxism is the para-functional movement of the mandible, occurring during the day or night. It can be associated with presence of audible sound when clenching or grinding the teeth. This is usually reported by parents or partners if the grinding occurs during sleep. In some cases, dental erosion is also associated with severe dental attrition. Dental erosion is tooth surface loss caused by extrinsic or intrinsic forms of acid. Extrinsic erosion is due to a highly acidic diet, while intrinsic erosion is caused by regurgitation of gastric acids. Erosion softens the dental hard tissues making them more susceptible to attrition. Thus, if erosion and bruxism both exist, surface loss due to attrition is faster. Severe attrition in young patients is usually associated with erosive factors in their diets. The different physiological processes of tooth wear (abrasion, attrition and erosion) usually occur simultaneously and rarely work individually. Therefore, it is important to understand these tooth wear processes and their interactions to determine causes of tooth surface loss. Demineralization of the tooth surface due to acids can cause occlusal erosion as well as attrition. Wedge-shaped cervical lesions are commonly found in association with occlusal erosion and attrition.

Tooth wear is typically seen in the elderly and can be referred to as a natural aging process. Attrition, abrasion, erosion or a combination of these factors are the main reasons for tooth wear in elderly people who retain their natural teeth. This tooth wear can be pathological or physiological. The number of teeth with incisal or occlusal wear increases with age. Attrition occurs in 1 in 3 adolescents.

In addition to other occlusal factors, independent variables such as male gender, bruxism, and loss of molar occlusal contact, edge-to-edge relation of incisors, unilateral buccolingual cusp-to-cusp relation, and unemployment have been identified in affecting occlusal wear. Similarly, anterior cross-bite, unilateral posterior cross-bite, and anterior crowding have been found to be protective factors for high occlusal wear levels.

Preventive and restorative care are important as well as esthetics as a consideration. This ensures preservation of the patient's vertical face height between their upper and lower teeth when they bite together. The basis of treatment is standard throughout the different types of DI where prevention, preservation of occlusal face height, maintenance of function, and aesthetic needs are priority. Preventive efforts can limit pathology occurring within the pulp, which may render future endodontic procedures less challenging, with better outcomes.

- Challenges are associated with root canal treatment of teeth affected by DI due to pulp chamber and root canal obliteration, or narrowing of such spaces.

- If root canal treatment is indicated, it should be done in a similar way like with any other tooth. Further consideration is given for restoring the root-treated tooth as it has weaker dentine which may not withstand the restoration.

Preservation of occlusal face height may be tackled by use of stainless steel crowns which are advocated for primary teeth where occlusal face height may be hugely compromised due to loss of tooth tissue as a result of attrition, erosion of enamel.

In most cases, full-coverage crowns or veneers (composite/porcelain) are needed for aesthetic appearance, as well as to prevent further attrition. Another treatment option is bonding, putting lighter enamel on the weakened enamel of the teeth and with lots of treatments of this bonding, the teeth appear whiter to the eye, but the teeth on the inside and under that cover are still the same. Due to the weakened condition of the teeth, many common cosmetic procedures such as braces and bridges are inappropriate for patients with Dentinogenesis imperfecta and are likely to cause even more damage than the situation they were intended to correct.

Dental whitening (bleaching) is contraindicated although it has been reported to lighten the color of DI teeth with some success; however, because the discoloration is caused primarily by the underlying yellow-brown dentin, this alone is unlikely to produce normal appearance in cases of significant discoloration.

If there is considerable attrition, overdentures may be prescribed to prevent further attrition of remaining teeth and for preserving the occlusal face height.

Feline Tooth Resorption (TR) is a syndrome in cats characterized by resorption of the tooth by odontoclasts, cells similar to osteoclasts. TR has also been called "feline odontoclastic resorption lesion" (FORL), neck lesion, cervical neck lesion, cervical line erosion, feline subgingival resorptive lesion, feline caries, or feline cavity. It is one of the most common diseases of domestic cats, affecting up to two-thirds. TRs have been seen more recently in the history of feline medicine due to the advancing ages of cats, but 800-year-old cat skeletons have shown evidence of this disease. Purebred cats, especially Siamese and Persians, may be more susceptible.

TRs clinically appear as erosions of the surface of the tooth at the gingival border. They are often covered with calculus or gingival tissue. It is a progressive disease, usually starting with loss of cementum and dentin and leading to penetration of the pulp cavity. Resorption continues up the dentinal tubules into the tooth crown. The enamel is also resorbed or undermined to the point of tooth fracture. Resorbed cementum and dentin is replaced with bone-like tissue.

The aetiology of dental abrasion can be due to a single stimuli or, as in most cases, multi-factorial. The most common cause of dental abrasion, is the combination of mechanical and chemical wear.

Tooth brushing is the most common cause of dental abrasion, which is found to develop along the gingival margin, due to vigorous brushing in this area. The type of toothbrush, the technique used and the force applied when brushing can influence the occurrence and severity of resulting abrasion. Further, brushing for extended periods of time (exceeding 2-3 min) in some cases, when combined with medium/hard bristled toothbrushes can cause abrasive lesions.

Different toothbrush types are more inclined to cause abrasion, such as those with medium or hard bristles. The bristles combined with forceful brushing techniques applied can roughen the tooth surface and cause abrasion as well as aggravating the gums. Repetitive irritation to the gingival margin can eventually cause recession of the gums. When the gums recede, the root surface is exposed which is more susceptible to abrasion.

Comparatively, electric toothbrushes have less abrasive tendencies.

Types of toothpastes can also damage enamel and dentine due to the abrasive properties. Specific ingredients are used in toothpaste to target removal of the bio-film and extrinsic staining however in some cases can contribute to the pastes being abrasive.

Whitening toothpastes are found to be one of the most abrasive types of toothpastes, according to the RDA Scale, detailed below. In-home and clinical whitening have been proven to increase the likelihood of an individual experiencing dental abrasion. It is believed that dental abrasion due to the whitening process is caused by a combination of both mechanical and chemical irritants, for example, using whitening toothpaste and at home bleaching kits together. However, if an individual is regimented in their after-whitening care then they can avoid loss of dentine minerals and in turn abrasion can be avoided. (that contribute to developing abrasion).

Another factor that can contribute to abrasion is alteration of pH levels in the saliva. This can be sugary/ acidic foods and liquids. The reasoning behind this is that an increase in acidity of saliva can induce demineralization and therefore compromising the tooth structure to abrasive factors such as tooth brushing or normal wear from mastication. When the tooth structure is compromised, this is where the mineral content of the saliva can create shallow depressions in the enamel and thus, when brushed can cause irreparable damage on tooth surface. The dental abrasion process can be further stimulated and accelerated through the effects of dental Acid erosion.

There are many possible causes of gingival bleeding. The main cause of gingival bleeding is the formation and accumulation of plaque at the gum line due to improper brushing and flossing of teeth. The hardened form of plaque is calculus. An advanced form of gingivitis as a result of formation of plaque is periodontitis. Other causes that can exacerbate gingival bleeding include:

- placement of new dentures

- tooth or gum infection

- diabetes mellitus

- idiopathic thrombocytopenic purpura

- leukemia

- malnutrition

- use of aspirin and anticoagulants(blood thinners) such as warfarin and heparin

- hormonal imbalances during puberty and pregnancy

- iron overload

Other less common causes are:

- vitamin C deficiency (scurvy) and vitamin K deficiency

- dengue fever

Treatment for TRs is limited to tooth extraction because the lesion is progressive. Amputation of the tooth crown without root removal has also been advocated in cases demonstrated on a radiograph to be type 2 resorption without associated periodontal or endodontic disease because the roots are being replaced by bone. However, X-rays are recommended prior to this treatment to document root resorption and lack of the periodontal ligament.

Tooth restoration is not recommended because resorption of the tooth will continue underneath the restoration. Use of alendronate has been studied to prevent TRs and decrease progression of existing lesions.

Dental attrition is a type of tooth wear caused by tooth-to-tooth contact, resulting in loss of tooth tissue, usually starting at the incisal or occlusal surfaces. Tooth wear is a physiological process and is commonly seen as a normal part of aging. Advanced and excessive wear and tooth surface loss can be defined as pathological in nature, requiring intervention by a dental practitioner. The pathological wear of the tooth surface can be caused by bruxism, which is clenching and grinding of the teeth. If the attrition is severe, the enamel can be completely worn away leaving underlying dentin exposed, resulting in an increased risk of dental caries and dentin hypersensitivity. It is best to identify pathological attrition at an early stage to prevent unnecessary loss of tooth structure as enamel does not regenerate.

Acidic drinks and foods lower the pH level of the mouth so consuming them causes the teeth to demineralise. Drinks low in pH levels that cause dental erosion include fruit juices, sports drinks, wine, beer and carbonated drinks. Orange and apple juices are common culprits among fruit juices. Carbonated drinks such as colas, lemonades are also very acidic, as are fruit-flavoured drinks and dilutables. Frequency rather than total intake of acidic juices is seen as the greater factor in dental erosion; infants using feeding bottles containing fruit juices (especially when used as a comforter) are therefore at greater risk of acid erosion.

Saliva acts as a buffer, regulating the pH when acidic drinks are ingested. Drinks vary in their resistance to the buffering effect of saliva. Studies show that fruit juices are the most resistant to saliva's buffering effect, followed by, in order: fruit-based carbonated drinks and flavoured mineral waters, non-fruit-based carbonated drinks, sparkling mineral waters; Mineral water being the least resistant. Because of this, fruit juices in particular, may prolong the drop in pH levels.

A number of medications such as vitamin C, aspirin and some iron preparations are acidic and may contribute towards acid erosion.