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.

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.

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.

Condylar resorption, also called idiopathic condylar resorption, ICR, and condylysis, is a temporomandibular joint disorder in which one or both of the mandibular condyles are broken down in a bone resorption process. This disorder is nine times more likely to be present in females than males, and is more common among teenagers.

The healing time for a routine mandible fractures is 4–6 weeks whether MMF or rigid internal fixation (RIF) is used. For comparable fractures, patients who received MMF will lose more weight and take longer to regain mouth opening, whereas, those who receive RIF have higher infection rates.

The most common long-term complications are loss of sensation in the mandibular nerve, malocclusion and loss of teeth in the line of fracture. The more complicated the fracture (infection, comminution, displacement) the higher the risk of fracture.

Condylar fractures have higher rates of malocclusion which in turn are dependent on the degree of displacement and/or dislocation. When the fracture is intracapsular there is a higher rate of late-term osteoarthritis and the potential for ankylosis although the later is a rare complication as long as mobilization is early. Pediatric condylar fractures have higher rates of ankylosis and the potential for growth disturbance.

Rarely, mandibular fracture can lead to Frey's syndrome.

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.

Jaw dislocation is common for people who are in car, motorcycle or related accidents and also sports related activities. This injury does not pin point specific ages or genders because it could happen to anybody. People who dislocate their jaw do not usually seek emergency medical care. In most cases, jaw dislocations are acute and can be altered by minor manipulations. It was reported from one study that over a seven-year period at an emergency medical site, with 100,000 yearly visits, there were only 37 patients that were seen for a dislocated jaw.

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.

Supracondylar humerus fractures account for 55%-75% of all elbow fractures. They most commonly occur in children between ages 5–8, because remodeling of bone in this age group causes a decreased supracondylar anteroposterior diameter.

Acroosteolysis is resorption of the distal bony phalanges. Acroosteolysis has two patterns of resorption in adults: diffuse and bandlike.

The diffuse pattern of resorption has a widely diverse differential diagnosis which includes: pyknodysostosis, collagen vascular disease and vasculitis, Raynaud's neuropathy, trauma, epidermolysis bullosa, psoriasis, frostbite, sarcoidosis, hypertrophic osteoarthropathy, acromegaly, and advanced leprosy.

The bandlike pattern of resorption may be seen with polyvinyl chloride exposure and Hadju-Cheney syndrome.

A mnemonic commonly used for acro-osteolysis is PINCHFO.

Pyknodysostosis, Psoriasis,

Injury (thermal burn, frostbite),

Neuropathy (diabetes),

Collagen vascular disease (scleroderma, Raynaud's),

Hyperparathyroidism,

Familial (Hadju-Cheney, progeria),

Occupational (polyvinyl exposure),

Acroosteolysis may be associated with minimal skin changes or with ischemic skin lesions that may result in digital necrosis.

Risk factors for osteoporotic fracture can be split between nonmodifiable and (potentially) modifiable. In addition, osteoporosis is a recognized complication of specific diseases and disorders. Medication use is theoretically modifiable, although in many cases, the use of medication that increases osteoporosis risk may be unavoidable.

Caffeine is not a risk factor for osteoporosis.

It is more likely in females than males.

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.

The temporomandibular joints (TMJ) are the two joints connecting the jawbone to the skull. It is a bilateral synovial articulation between the temporal bone of the skull above and the mandible below; it is from these bones that its name is derived.

Hip fractures are responsible for the most serious consequences of osteoporosis. In the United States, more than 250,000 hip fractures annually are attributable to osteoporosis. A 50-year-old white woman is estimated to have a 17.5% lifetime risk of fracture of the proximal femur. The incidence of hip fractures increases each decade from the sixth through the ninth for both women and men for all populations. The highest incidence is found among men and women ages 80 or older.

Most temporomandibular disorders (TMDs) are self-limiting and do not get worse. Simple treatment, involving self-care practices, rehabilitation aimed at eliminating muscle spasms, and restoring correct coordination, is all that is required. Nonsteroidal anti inflammatory analgesics (NSAIDs) should be used on a short-term, regular basis and not on an as needed basis. On the other hand, treatment of chronic TMD can be difficult and the condition is best managed by a team approach; the team consists of a primary care physician, a dentist, a physiotherapist, a psychologist, a pharmacologist, and in small number of cases, a surgeon. The different modalities include patient education and self-care practices, medication, physical therapy, splints, psychological counseling, relaxation techniques, biofeedback, hypnotherapy, acupuncture, and arthrocentesis.

As with most dislocated joints, a dislocated jaw can usually be successfully positioned into its normal position by a trained medical professional. Attempts to readjust the jaw without the assistance of a medical professional could result in worsening of the injury. The health care provider may be able to set it back into the correct position by manipulating the area back into its proper position. Numbing medications such as general anesthetics, muscle relaxants, or in some cases sedation, may be needed to relax the strong jaw muscle. In more severe cases, surgery may be needed to reposition the jaw, particularly if repeated jaw dislocations have occurred.

The medication(s) listed below have been approved by the Food and Drug Administration (FDA) as orphan products for treatment of this condition. Learn more orphan products.

Giant osteoclasts can occur in some diseases, including Paget's disease of bone and bisphosphonate toxicity.

To date, the specific cause of Gorham's disease remains unknown.

Bone mass and strength are obtained and maintained through a process of bone destruction and replacement that occurs at the cellular level throughout a person's life. Cells called osteoclasts secrete enzymes that dissolve old bone, allowing another type of cells called osteoblasts to form new bone. Except in growing bone, the rate of breakdown equals the rate of building, thereby maintaining bone mass. In Gorham's disease that process is disrupted.

Gorham and Stout found that vascular anomalies always occupied space that normally would be filled with new bone and speculated that the presence of angiomatosis may lead to chemical changes in the bone. Gorham and others speculated that such a change in the bone chemistry might cause an imbalance in the rate of osteoclast activity to osteoblast activity such that more bone is dissolved than is replaced. Beginning in the 1990s there were reports of elevated levels of a protein called interleukin-6 (IL-6) being detected in patients with the disease, leading some to suggest that increased levels of IL-6 and vascular endothelial growth factor (VEGF) may contribute to the chemical changes Gorham and others believed were the cause of this type of osteolysis.

In 1999 Möller and colleagues concluded, "The Gorham-Stout syndrome may be, essentially, a monocentric bone disease with a focally increased bone resorption due to an increased number of paracrine – or autocrine – stimulated hyperactive osteoclasts. The resorbed bone is replaced by a markedly vascularized fibrous tissue. The apparent contradiction concerning the presence or absence or the number of osteoclasts, may be explained by the different phases of the syndrome." They further stated that their histopathological study provided good evidence that osteolytic changes seen in Gorham's disease are the result of hyperactive osteoclastic bone. However, others have concluded that lymphangiomatosis and Gorham's disease should be considered as a spectrum of disease rather than separate diseases.

While there is consensus that Gorham's is caused by deranged osteoclastic activity, there is not yet conclusive evidence as to what causes this deranged behavior to begin.

The Pink and Pulseless hand in supracondylar fracture has been assigned the following causes:

1. tear or entrapment of the brachial artery

2. spasm of the artery and

3. compression of the artery relieved by manipulation of the fracture

4. compression of median nerve.

Thus there is loss of circulation of forearm, causing lack of reperfusion of tissues resulting in tissue death causing compartment syndrome.

Therefore, the complications of elbow dislocations include the following:

- Posttraumatic periarticular calcification, which occurs in 3-5% of elbow injuries

- Myositis ossificans or calcific tendinitis

- Neurovascular injuries (8-21% of cases) — palsy to the anterior interosseus nerve at time of index injury is most common, followed by brachial artery injuries (5-13%). Injury to the ulnar nerve is reported with percutaneous pinning through the medial epicondyle.

- Osteochondral defects, intra-articular loose bodies, and avascular necrosis of the capitulum

- Instability

Calcific tendinitis is a form of tendinitis, a disorder characterized by deposits of hydroxyapatite (a crystalline calcium phosphate) in any tendon of the body, but most commonly in the tendons of the rotator cuff (shoulder), causing pain and inflammation. The condition is related to and may cause adhesive capsulitis ("frozen shoulder").

In reality, both of these mechanisms probably play a role in the development of a Charcot joint.

Gorham's disease (pronounced GOR-amz), also known as Gorham vanishing bone disease and phantom bone disease, is a very rare skeletal condition of unknown cause, characterized by the uncontrolled proliferation of distended, thin-walled vascular or lymphatic channels within bone, which leads to resorption and replacement of bone with angiomas and/or fibrosis. Current treatments are experimental only.

Any condition resulting in decreased peripheral sensation, proprioception, and fine motor control:

- Diabetes mellitus neuropathy (the most common in the U.S. today, resulting in destruction of foot and ankle joints), with Charcot joints in 1/600-700 diabetics. Related to long-term poor glucose control.

- Alcoholic neuropathy

- Cerebral palsy

- Leprosy

- Syphilis ("tabes dorsalis"), caused by the organism "Treponema pallidum"

- Spinal cord injury

- Myelomeningocele

- Syringomyelia

- Intra-articular steroid injections

- Congenital insensitivity to pain

- Peroneal muscular atrophy

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.