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

OM is usually a polymicrobial, opportunistic infection, caused primarily by a mixture of alpha hemolytic streptococci and anaerobic bacteria from the oral cavity such as "Peptostreptococcus", "Fusobacterium" and "Prevotella", (in contrast to OM of the long bones, usually caused by isolated "Staphylococcus aureus" infection). These are the same as the common causative organisms in odotonogenic infections. However, when OM in the jaws follows trauma, is the likely cause is still staphylococcal (usually "Staphylococcus epidermis".

Other risk factors can be any familial hypercoagulation tendency, including for example, Factor V (Five) Leiden heterozygosity.

Smoking and tobacco use of any kind are associated with increased risk of dry socket. This may be partially due to the vasoconstrictive action of nicotine on small blood vessels. Abstaining from smoking in the days immediately following a dental extraction reduces the risk of a dry socket occurring.

Overall, the incidence of dry socket is about 0.5–5% for routine dental extractions, and about 25–30% for impacted mandibular third molars (wisdom teeth which are buried in the bone).

Females are more frequently affected than males, but this appears to be related to oral contraceptive use rather than any underlying gender predilection. The majority of dry sockets occur in individuals aged between 20 and 40 which is when most dental extractions occur, although for any given individual it is more likely to occur in with increasing age.

Other possible risk factors include periodontal disease, acute necrotizing ulcerative gingivitis, local bone disease, Paget's disease of bone, osteopetrosis, cemento-osseous dysplasia, a history of previously developing a dry socket with past extractions and inadequate oral hygiene. Other factors in the postoperative period that may lead to loss of the blood clot include forceful spitting, sucking through a straw, and coughing or sneezing.

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.

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.

Infection of periapical tissues of a high immunity host by organisms of low virulence which leads to a localized bony reaction to a low grade inflammatory stimulus.

Condensing osteitis is a periapical inflammatory disease that results from a reaction to a dental related infection. This causes more bone production rather than bone destruction in the area (most common site is near the root apices of premolars and molars). The lesion appears as a radiopacity in the periapical area hence the sclerotic reaction. The sclerotic reaction results from good patient immunity and a low degree of virulence of the offending bacteria. The associated tooth may be carious or contains a large restoration, and is usually associated with a non-vital tooth.

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.

A reaction to past trauma or infection but it's difficult to rule out in some cases.

Osteitis is inflammation of bone. More specifically, it can refer to one of the following conditions:

- Osteomyelitis, or "infectious osteitis", mainly "bacterial osteitis")

- Alveolar osteitis or "dry socket"

- Condensing osteitis (or Osteitis condensans)

- Osteitis deformans (or Paget's disease of bone)

- Osteitis fibrosa cystica (or Osteitis fibrosa, or Von Recklinghausen's disease of bone)

- Osteitis pubis

- Radiation osteitis

- Osteitis condensans ilii

- Panosteitis, a long bone condition in large breed dogs

- In horses, pedal osteitis is frequently confused with laminitis.

The prognosis for impacted wisdom teeth depends on the depth of the impaction. When they lack a communication to the mouth, the main risk is the chance of cyst or neoplasm formation which is relatively uncommon.

Once communicating with the mouth, the onset of disease or symptoms cannot be predicted but the chance of it does increase with age. Less than 2% of wisdom teeth are free of either periodontal disease or caries by age 65. Further, several studies have found that between 30% – 60% of people with previously asymptomatic impacted wisdom teeth will have them extracted due to symptoms or disease, 4–12 years after initial examination.

Extraction of the wisdom teeth removes the disease on the wisdom tooth itself and also appears to improve the periodontal status of the second molar, although this benefit diminishes beyond the age of 25.

A sequestrum (plural: sequestra) is a piece of dead bone that has become separated during the process of necrosis from normal or sound bone.

It is a complication (sequela) of osteomyelitis. The pathological process is as follows:

- infection in the bone leads to an increase in intramedullary pressure due to inflammatory exudates

- the periosteum becomes stripped from the osteum, leading to vascular thrombosis

- bone necrosis follows due to lack of blood supply

- sequestra are formed

The sequestra are surrounded by sclerotic bone which is relatively avascular (without a blood supply). Within the bone itself, the haversian canals become blocked with scar tissue, and the bone becomes surrounded by thickened periosteum.

Due to the avascular nature of this bone, antibiotics which travel to sites of infection via the bloodstream poorly penetrate these tissues, hence the difficulty in treating chronic osteomyelitis.

At the same time as this, new bone is forming (known as involucrum). Openings in this involucrum allow debris and exudates (including pus) to pass from the sequestrum via sinus tracts to the skin.

Rarely, a sequestrum may turn out to be an osteoid osteoma, a rare tumor of the bone.

Osteomyelitis (OM) is an infection of bone. Symptoms may include pain in a specific bone with overlying redness, fever, and weakness. The long bones of the arms and legs are most commonly involved in children while the feet, spine, and hips are most commonly involved in adults.

The cause is usually a bacterial infection and rarely a fungal infection. It may occur via spread from the blood or from surrounding tissue. Risks for developing osteomyelitis include diabetes, intravenous drug use, prior removal of the spleen, and trauma to the area. Diagnosis is typically suspected based on symptoms. This is then supported by blood tests, medical imaging, or bone biopsy.

Treatment often involves both antimicrobials and surgery. In those with poor blood flow, amputation may be required. With treatment outcomes are often generally good when the condition has only been present a short time. About 2.4 per 100,000 people are affected a year. The young and old are more commonly affected. Males are more commonly affected than females. The condition was described at least as early as the 300s BC by Hippocrates. Before the availability of antibiotics the risk of death was significant.

In children, the long bones are usually affected. In adults, the vertebrae and the pelvis are most commonly affected.

Acute osteomyelitis almost invariably occurs in children because of rich blood supply to the growing bones. When adults are affected, it may be because of compromised host resistance due to debilitation, intravenous drug abuse, infectious root-canaled teeth, or other disease or drugs (e.g., immunosuppressive therapy).

Osteomyelitis is a secondary complication in 1–3% of patients with pulmonary tuberculosis. In this case, the bacteria, in general, spread to the bone through the circulatory system, first infecting the synovium (due to its higher oxygen concentration) before spreading to the adjacent bone. In tubercular osteomyelitis, the long bones and vertebrae are the ones that tend to be affected.

"Staphylococcus aureus" is the organism most commonly isolated from all forms of osteomyelitis.

Bloodstream-sourced osteomyelitis is seen most frequently in children, and nearly 90% of cases are caused by "Staphylococcus aureus". In infants, "S. aureus", Group B streptococci (most common) and "Escherichia coli" are commonly isolated; in children from one to 16 years of age, "S. aureus", "Streptococcus pyogenes", and "Haemophilus influenzae" are common. In some subpopulations, including intravenous drug users and splenectomized patients, Gram-negative bacteria, including enteric bacteria, are significant pathogens.

The most common form of the disease in adults is caused by injury exposing the bone to local infection. "Staphylococcus aureus" is the most common organism seen in osteomyelitis, seeded from areas of contiguous infection. But anaerobes and Gram-negative organisms, including "Pseudomonas aeruginosa", "E. coli", and "Serratia marcescens", are also common. Mixed infections are the rule rather than the exception.

Systemic mycotic (fungal) infections may also cause osteomyelitis. The two most common are "Blastomyces dermatitidis" and "Coccidioides immitis".

In osteomyelitis involving the vertebral bodies, about half the cases are due to "S. aureus", and the other half are due to tuberculosis (spread hematogenously from the lungs). Tubercular osteomyelitis of the spine was so common before the initiation of effective antitubercular therapy, it acquired a special name, Pott's disease.

The "Burkholderia cepacia" complex has been implicated in vertebral osteomyelitis in intravenous drug users.

Females are affected more than males, and the condition occurs in permanent (adult) teeth more than deciduous (baby teeth or milk teeth).

Few studies have looked at the percentage of the time wisdom teeth are present or the rate of wisdom teeth eruption. The lack of up to five teeth (excluding third molars, i.e. wisdom teeth) is termed hypodontia. Missing third molars occur in 9-30% of studied populations.

One large scale study on a group of young adults in New Zealand showed 95.6% had at least 1 wisdom tooth with an eruption rate of 15% in the maxilla and 20% in the mandible. Another study on 5000 army recruits found 10,767 impacted wisdom teeth. The frequency of impacted lower third molars has been found to be 72% and the frequency of retained impacted wisdom teeth that are free of disease and symptoms is estimated at 11.6% to 29% which drops with age.

The incidence of wisdom tooth removal was estimated to be 4 per 1000 person years in England and Wales prior to the 2000 NICE guidelines.

Extra teeth, lost teeth, impacted teeth, or abnormally shaped teeth have been cited as causes of malocclusion. A small underdeveloped jaw, caused by lack of masticatory stress during childhood, can cause tooth overcrowding. Ill-fitting dental fillings, crowns, appliances, retainers, or braces as well as misalignment of jaw fractures after a severe injury are other causes. Tumors of the mouth and jaw, thumb sucking, tongue thrusting, pacifier use beyond age 3, and prolonged use of a bottle have also been identified as causes.

In an experiment on two groups of rock hyraxes fed hardened or softened versions of the same foods, the animals fed softer food had significantly narrower and shorter faces and thinner and shorter mandibles than animals fed hard food. Experiments have shown similar results in other animals, including primates, supporting the theory that masticatory stress during childhood affects jaw development. Several studies have shown this effect in humans. Children chewed a hard resinous gum for two hours a day and showed increased facial growth.

During the transition to agriculture, the shape of the human mandible went through a series of changes. The mandible underwent a complex series of shape changes not matched by the teeth, leading to incongruity between dental and mandibular form. These changes in human skulls may have been "driven by the decreasing bite forces required to chew the processed foods eaten once humans switched to growing different types of cereals, milking and herding animals about 10,000 years ago."

Traumatic bone cyst, also called a simple bone cyst, is a condition of the jaws. It is more likely to affect men and is more likely to occur in people in their first and second decades. There is no known cause though it is sometimes related to trauma. It appears on radiographs as a well-circumscribed radiolucency (dark area), and it commonly scallops between the roots of teeth. When the lesion is surgically opened, an empty cavity is found.

One study showed female predominance.

Crowding of the teeth is treated with orthodontics, often with tooth extraction, clear aligners, or dental braces, followed by growth modification in children or jaw surgery (orthognathic surgery) in adults. Surgery may be required on rare occasions. This may include surgical reshaping to lengthen or shorten the jaw (orthognathic surgery). Wires, plates, or screws may be used to secure the jaw bone, in a manner similar to the surgical stabilization of jaw fractures. Very few people have "perfect" alignment of their teeth. However, most problems are very minor and do not require treatment.

A Brodie abscess is a subacute osteomyelitis, which may persist for years before converting to a frank osteomyelitis. Classically, this may present after conversion as a draining abscess extending from the tibia out through the shin. Occasionally acute osteomyelitis may be contained to a localized area and walled off by fibrous and granulation tissue. This is termed Brodie's abscess.

Most frequent causative organism is Staphylococcus aureus.

The prognosis depends upon the type, size and location of a cyst. Most cysts are entirely benign, and some may require no treatment. Rarely, some cystic lesions represent locally aggressive tumors that may cause destruction of surrounding bone if left untreated. This type of cyst are usually removed with a margin of healthy bone to prevent recurrence of new cysts. If a cyst expands to a very large size, the mandible may be weakened such that a pathologic fracture occurs.

Radicular cysts are by far the most common cyst occurring in the jaws.

Mainly surgical approach has to be taken.

If cavity is small then surgical evacuation & curettage is performed under antibiotic cover.

If cavity is large then after evacuation, packing with cancellous bone chips

Loss of attachment:

- By far the most common cause is periodontal disease (gum disease). This is painless, slowly progressing loss of bony support around teeth. It is made worse by smoking and the treatment is by improving the oral hygiene above and below the gumline.

- Dental abscesses can cause resorption of bone and consequent loss of attachment. Depending on the type of abscess, this loss of attachment may be restored once the abscess is treated, or it may be permanent.

- Many other conditions can cause permanent or temporary loss of attachment and increased tooth mobility. Examples include: Langerhans cell histiocytosis.

Increased forces on the tooth:

- Bruxism (abnormal clenching and grinding of teeth) can aggravate attachment loss and tooth mobility if periodontal disease is already present. The tooth mobility is typically reversible and the tooth returns to normal level of mobility once the bruxism is controlled.

- Dental trauma. Luxations, and root fractures of teeth can cause sudden mobility after a blow. Dental trauma may be isolated or associated with other facial trauma.

- Increased biting force on one tooth can cause temporary increased mobility until corrected. A common scenario is a new filling or crown which is a fraction of a millimeter too prominent in the bite, which after a few days causes periodontal pain in that tooth and/or the opposing tooth.