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.

The treatment should be tailored to the cause involved and the severity of the disease process. With oral osteoporosis the emphasis should be on good nutrient absorption and metabolic wastes elimination through a healthy gastro-intestinal function, effective hepatic metabolism of toxicants such as exogenous estrogens, endogenous acetaldehyde and heavy metals, a balanced diet, healthy lifestyle, assessment of factors related to potential coagulopathies, and treatment of periodontal diseases and other oral and dental infections.

In cases of advanced oral ischaemic osteoporosis and/or ONJ that are not bisphosphonates related, clinical evidence has shown that surgically removing the damaged marrow, usually by curettage and decortication, will eliminate the problem (and the pain) in 74% of patients with jaw involvement. Repeat surgeries, usually smaller procedures than the first, may be required. Almost a third of jawbone patients will need surgery in one or more other parts of the jaws because the disease so frequently present multiple lesions, i.e., multiple sites in the same or similar bones, with normal marrow in between. In the hip, at least half of all patients will get the disease in the opposite hip over time; this pattern occurs in the jaws as well. Recently, it has been found that some osteonecrosis patients respond to anticoagulation therapies alone. The earlier the diagnosis the better the prognosis. Research is ongoing on other non-surgical therapeutic modalities that could alone or in combination with surgery further improve the prognosis and reduce the morbidity of ONJ. A greater emphasis on minimizing or correcting known causes is necessary while further research is conducted on chronic ischaemic bone diseases such as oral osteoporosis and ONJ.

In patients with bisphosphonates-associated ONJ, the response to surgical treatment is usually poor. Conservative debridement of necrotic bone, pain control, infection management, use of antimicrobial oral rinses, and withdrawal of bisphosphonates are preferable to aggressive surgical measures for treating this form of ONJ. Although an effective treatment for bisphosphonate-associated bone lesions has not yet been established, and this is unlikely to occur until this form of ONJ is better understood, there have been clinical reports of some improvement after 6 months or more of complete cessation of bisphosphonate therapy.

Culture and sensitivity of the wound site determines the choice of antibiotic. Repeated culture and sensitivity testing is often carried out in OM since the treatment is prolonged and antibiotic resistance may occur, when a change in the drug may be required.

Pathologic fracture of the mandible is a possible complication of OM where the bone has been weakened significantly.

Treatment of condylar resorption is controversial. Orthognathic surgery may be done to reconstruct and stabilize the condyles and disc of the temporomandibular joint. Anti-infammatory medication is also used to slow the resorption process. Orthodontics may be used to treat the occlusion. Arthrocentesis, and arthroscopic surgery are also sometimes used to treat disc displacement and other symptoms.

While bone resorption is commonly associated with many diseases or joint problems, the term "osteolysis" generally refers to a problem common to artificial joint replacements such as total hip replacements, total knee replacements and total shoulder replacements. Osteolysis can also be associated with the radiographic changes seen in those with bisphosphonate-related osteonecrosis of the jaw.

There are several biological mechanisms which may lead to osteolysis. In total hip replacement, the generally accepted explanation for osteolysis involves wear particles (worn off the contact surface of the artificial ball and socket joint). As the body attempts to clean up these wear particles (typically consisting of plastic or metal), it triggers an autoimmune reaction which causes resorption of living bone tissue. Osteolysis has been reported to occur as early as 12 months after implantation and is usually progressive. This may require a revision surgery (replacement of the prosthesis).

Although osteolysis itself is clinically asymptomatic, it can lead to implant loosening or bone breakage, which in turn causes serious medical problems.

The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding takes place after an injury as well as during normal growth. Normally, bone continuously breaks down and rebuilds—old bone is resorbed and replaced with new bone. The process keeps the skeleton strong and helps it to maintain a balance of minerals. In the course of avascular necrosis, however, the healing process is usually ineffective and the bone tissues break down faster than the body can repair them. If left untreated, the disease progresses, the bone collapses, and the joint surface breaks down, leading to pain and arthritis.

A variety of methods may be used to treat the most common being the total hip replacement (THR). However, THRs have a number of downsides including long recovery times and short life spans (of the hip joints). THRs are an effective means of treatment in the older population; however, in younger people they may wear out before the end of a person's life.

Other technicques such as metal on metal resurfacing may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. Bisphosphonates which reduces the rate of bone breakdown may prevent collapse (specifically of the hip) due to AVN.

Osteoradionecrosis is a possible complication following radiotherapy where an area of bone does not heal from irradiation. Irradiation of bones causes damage to osteocytes and impairs the blood supply. The affected hard tissues become hypovascular (reduced number of blood vessels), hypocellular (reduced number of cells) and hypoxic (low levels of oxygen). Osteoradionecrosis usually occurs in the mandible, and causes chronic pain and surface ulceration. Prevention of osteradionecrosis is part of the reason all teeth of questionable prognosis are removed before the start of a course of radiotherapy.

Osteoradionecrosis of the jaw is a significant complication of radiotherapy for oral cavity cancer. In addition to antibiotic medication, treatment options such as hyperbaric oxygen therapy, surgical approaches, and combined therapy with pentoxifylline and tocopherol have been introduced.

Generally buccal exostoses require no treatment. However, they may be easily traumatized causing ulceration, or may contribute to periodontal disease if they become too large, or can interfere with wearing a denture (false teeth). If they are creating problems, they are generally removed with a simple surgical procedure under local anesthetic.

Osteolysis is an active resorption of bone matrix by osteoclasts and can be interpreted as the reverse of ossification. Although osteoclasts are active during the natural formation of healthy bone the term "osteolysis" specifically refers to a pathological process. Osteolysis often occurs in the proximity of a prosthesis that causes either an immunological response or changes in the bone's structural load. Osteolysis may also be caused by pathologies like bone tumors, cysts, or chronic inflammation.

Mandible fracture causes vary by the time period and the region studied. In North America, blunt force trauma (a punch) is the leading cause of mandible fracture whereas in India, motor vehicle collisions are now a leading cause. On battle grounds, it is more likely to be high velocity injuries (bullets and shrapnel). Prior to the routine use of seat belts, airbags and modern safety measures, motor vehicle collisions were a leading cause of facial trauma. The relationship to blunt force trauma explains why 80% of all mandible fractures occur in males. Mandibular fracture is a rare complication of third molar removal, and may occur during the procedure or afterwards. With respect to trauma patients, roughly 10% have some sort of facial fracture, the majority of which come from motor vehicle collisions. When the person is unrestrained in a car, the risk of fracture rises 50% and when an unhelmeted motorcyclist the risk rises 4-fold.

Like all fractures, consideration has to be given to other illnesses that might jeopardize the patient, then to reduction and fixation of the fracture itself. Except in avulsive type injuries, or those where there might be airway compromise, a several day delay in the treatment of mandible fractures seems to have little impact on the outcome or complication rates.

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.

A related condition, bisphosphonate-associated osteonecrosis of the jaw (BON), has been described as a side-effect of amino-bisphosphonates, a class of phosphorus-based drugs that inhibit bone resorption and are used widely for treating osteoporosis, bone disease in cancer and some other conditions.

BON, sometimes called "bis-phossy jaw",

is primarily associated with the use of intravenous bisphosphonates in the treatment of cancer. The percentage incidence of BON from this use is approximately 1000 times higher than the incidence of BON caused by the use of oral bisphosphonates.

Idiopathic osteosclerosis is a condition which may be found around the roots of a tooth. It is usually painless and found during routine radiographs. It appears as a radiopaque (light area) around a tooth, usually a premolar or molar. There is no sign of inflammation of the tooth.

Bisphosphonates have recently been introduced to treat several bone disorders, which include osteogenesis imperfecta.

A recognized risk of this drug relevant to dental treatments is bisphosphonate-associated osteonecrosis of the jaw (BRONJ). Occurrences of this risk is associated with dental surgical procedures such as extractions.

Dental professionals should therefore proceed with caution when carrying out any dental procedures in patients who have Type 2 DI who may be on bisphosphonate drug therapy.

Condylar resorption is an idiopathic condition, though there are some theories relating to its possible cause. Because condylar resorption is more likely to be in young females, hormonal mediation may be involved. Strain on the temporomandibular joint from orthodontics or orthognathic surgery may be related to the condition. Reactive arthritis, rheumatoid arthritis, and psoriatic arthritis are other possible causes.

If the diver has not been exposed to excessive depth and decompression and presents as DON, there may be a predisposition for the condition. Diving should be restricted to shallow depths. Divers who have suffered from DON are at increased risk of future fracture of a juxta-articular lesion during a dive, and may face complications with future joint replacements. Because of the young age of the population normally affected, little data is available regarding joint replacement complications.

There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental or helium diving. Physically stressful diving should probably be restricted, both in sport diving and work diving due to the possibility of unnecessary stress to the joint. Any diving should be less than 40 feet/12 meters. These risks are affected by the degree of disability and by the type of lesion (juxta-articular or shaft).

Condensing osteitis, sclerosing osteomyelitis, cementoblastoma, hypercementosis, Exostoses (tori).

Condensing osteitis may resemble idiopathic osteosclerosis, however, associated teeth are always nonvital in condensing osteitis.

They are more common in males than females, occurring in a ratio of about 5:1. They are strongly associated with the presence of torus mandibularis and torus palatinus.

Pycnodysostosis (from Greek: πυκνός (puknos) meaning "dense", "dys" ("defective"), and "ostosis" ("condition of the bone")), is a lysosomal storage disease of the bone caused by a mutation in the gene that codes the enzyme cathepsin K.

Craniomandibular osteopathy, also known as lion's jaw, is a developmental disease in dogs causing extensive bony changes in the mandible and skull. In this disease, a cyclical resorption of normal bone and replacement by immature bone occurs along the inner and outer surfaces of the affected bones. It usually occurs between the ages of 3 and 8 months. Breeds most commonly affected include the West Highland White Terrier, Scottish Terrier, Cairn Terrier, and Boston Terrier. It is rare in large-breed dogs, but it has been reported. Symptoms include firm swelling of the jaw, drooling, pain, and difficulty eating.

It is an inherited disease, especially in Westies, in which it has been recognized as an autosomal recessive trait. Canine distemper has also been indicated as a possible cause, as has "E. coli" infection, which could be why it is seen occasionally in large-breed dogs. Growth of lesions will usually stop around the age of one year, and possibly regress. This timing coincides with the normal completion of endochondral bone growth and ossification. If the disease is extensive, especially around the tympanic bulla (middle ear), then the prognosis is guarded.

A similar disease seen in young Bullmastiffs is known as calvarial hyperostotic syndrome. It is also similar to human infantile cortical hyperostosis. It is characterized by irregular, progressive bony proliferation and thickening of the cortical bone of the calvaria, which is part of the skull. Asymmetry of the lesions may occur, which makes it different from craniomandibular osteopathy. Symptoms include painful swelling of the skull, fever, and lymph node swelling. In most cases it is self-limiting.

Neuralgia-inducing cavitational osteonecrosis (NICO) is a controversial diagnosis whereby a putative jawbone cavitation causes chronic facial neuralgia; this is different from osteonecrosis of the jaw.. In NICO the pain is said to result from the degenerating nerve ("neuralagia"). The condition is probably rare, if it does exist.

Also called Ratner's bone cavity, a neuralgia-inducing cavitational osteonecrosis was first described in dental literature by G V Black in 1920. Several decades later, oral pathologist Jerry E Bouquot took especial interest in NICO.

The diagnostic criteria for NICO are imprecise, and the research offered to support it is flawed. The diagnosis is popular among holistic dentists who attempt to treat NICO by surgically removing the dead bone they say is causing the pain.

It has been rejected as quackery by some dentists and maxillofacial surgeons. In its position statement, dated 1996, the American Association of Endodontists asserted that although NICO occur and are treatable in toothless areas, NICO occurrence and treatment at endodontically treated teeth is generally implausible, that the diagnosis ought to be a last resort, and that routine extraction of endodontically treated teeth is misguided.

This is an autosomal recessive osteochondrodysplasia that maps to chromosome 1q21. Deficiency of Cathepsin K, a cysteine protease in osteoclasts, is known to cause this condition. Cathepsin K became a much sought-after drug target in osteoporosis after the cause of pycnodysostosis was discovered. The disease consistently causes short stature. The height of adult males with the disease is less than . Adult females with the syndrome are even shorter.

The disease has been named Toulouse-Lautrec syndrome, after the French artist Henri de Toulouse-Lautrec, who may have had the disease. In 1996, the defective gene responsible for pycnodysostosis was located, offering accurate diagnosis, carrier testing and a more thorough understanding of this disorder.