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."

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.

Teeth are constantly subject to both horizontal and vertical occlusal forces. With the center of rotation of the tooth acting as a fulcrum, the surface of bone adjacent to the pressured side of the tooth will undergo resorption and disappear, while the surface of bone adjacent to the tensioned side of the tooth will undergo apposition and increase in volume.

In both primary and secondary occlusal trauma, tooth mobility might develop over time, with it occurring earlier and being more prevalent in secondary occlusal trauma. To treat mobility due to primary occlusal trauma, the cause of the trauma must be eliminated. Likewise for teeth subject to secondary occlusal trauma, though these teeth may also require splinting together to the adjacent teeth so as to eliminate their mobility.

In primary occlusal trauma, the cause of the mobility was the excessive force being applied to a tooth with a normal attachment apparatus, otherwise known as a "periodontally-uninvolved tooth". The approach should be to eliminate the cause of the pain and mobility by determining the causes and removing them; the mobile tooth or teeth will soon cease exhibiting mobility. This could involve removing a high spot on a recently restored tooth, or even a high spot on a non-recently restored tooth that perhaps moved into hyperocclusion. It could also involve altering one's parafunctional habits, such as refraining from chewing on pens or biting one's fingernails. For a bruxer, treatment of the patient's primary occlusal trauma could involve selective grinding of certain interarch tooth contacts or perhaps employing a nightguard to protect the teeth from the greater than normal occlusal forces of the patient's parafunctional habit. For someone who is missing enough teeth in non-strategic positions so that the remaining teeth are forced to endure a greater "per square inch" occlusal force, treatment might include restoration with either a removable prosthesis or implant-supported crown or bridge.

In secondary occlusal trauma, simply removing the "high spots" or selective grinding of the teeth will not eliminate the problem, because the teeth are already periodontally involved. After splinting the teeth to eliminate the mobility, the cause of the mobility (in other words, the loss of clinical attachment and bone) must be managed; this is achieved through surgical periodontal procedures such as soft tissue and bone grafts, as well as restoration of edentulous areas. As with primary occlusal trauma, treatment may include either a removable prosthesis or implant-supported crown or bridge.

Secondary occlusal trauma occurs when "normal or excessive occlusal forces" are placed on teeth with "compromised periodontal attachment", thus contributing harm to an already damaged system. As stated, secondary occlusal trauma occurs when there is a compromised periodontal attachment and, thus, a "pre-existing periodontal condition".

The Kennedy classification quantifies partial edentulism. An outline is covered at the removable partial denture article.

The etiology, or cause of edentulism, can be multifaceted. While the extraction of non-restorable or non-strategic teeth by a dentist does contribute to edentulism, the predominant cause of tooth loss in developed countries is periodontal disease. While the teeth may remain completely decay-free, the bone surrounding and providing support to the teeth may reabsorb and disappear, giving rise to tooth mobility and eventual tooth loss. In the radiograph at the beginning of the article, tooth #21 (the lower left first premolar, to the right of #22, the lower left canine) exhibits 50% bone loss, presenting with a distal horizontal defect and a mesial vertical defect. Tooth #22 exhibits roughly 30% bone loss.

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.

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.

In disease states, maxillary prognathism is associated with Cornelia de Lange syndrome; however, so-called false maxillary prognathism, or more accurately, retrognathism, where there is a lack of growth of the mandible, is by far a more common condition.

Prognathism, if not extremely severe, can be treated in growing patients with orthodontic functional or orthopaedic appliances. In adult patients this condition can be corrected by means of a combined surgical/orthodontic treatment, where most of the time a mandibular advancement is performed. The same can be said for mandibular prognathism.

Not all alveolar prognathism is anomalous, and significant differences can be observed among different ethnic groups.

Harmful habits such as thumb sucking or tongue thrusting can result in or exaggerate an alveolar prognathism, causing teeth to misalign. Functional appliances can be used in growing children to help modify bad habits and neuro-muscular function, with the aim of correcting this condition.

Alveolar prognathism can also easily be corrected with fixed orthodontic therapy. However, relapse is quite common, unless the cause is removed or a long-term retention is used.

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.

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.

Brachygnathism or colloquially Parrot Mouth, is the uneven alignment of the upper and lower teeth in horses. In serious cases, the upper teeth protrude beyond the lower teeth. Problem with parrot mouth occur if the molars at the back of the mouth are also uneven, resulting in large hooks forming on the upper molars and the rear of the lower back molars. Horses with parrot mouth often require dental treatment at least every six months to remove the hooks and maintain alignment.

The equivalent conditions in humans are termed retrognathism or prognathism depending on whether the lower jaw is too far back or too far forward respectively.

Dilaceration is a developmental disturbance in shape of teeth. It refers to an angulation, or a sharp bend or curve, in the root or crown of a formed tooth.

The condition is thought to be due to trauma or possibly a delay in tooth eruption relative to bone remodeling gradients during the period in which tooth is forming. The result is that the position of the calcified portion of the tooth is changed and the remainder of the tooth is formed at an angle.

The curve or bend may occur anywhere along the length of the tooth, sometimes at the cervical portion, at other times midway along the root or even just at the apex of the root, depending upon the amount of root formed when the injury occurred.

Such an injury to a permanent tooth, resulting in dilaceration, often follows traumatic injury to the deciduous predecessor in which that tooth is driven apically into the jaw.

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

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

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

A diastema (plural diastemata) is a space or gap between two teeth. Many species of mammals have diastemata as a normal feature, most commonly between the incisors and molars. Diastemata are common for children and can exist in adult teeth as well. Diastemata are primarily caused by imbalance in the relationship between the jaw and the size of teeth. If the labial frenulum (lip tissue) pulls, it can also push the teeth apart and cause a diastema between the center of the two front teeth.

The adaptation from nasal to mouth breathing takes pace when changes such as chronic middle ear infections, sinusitis, allergic rhinitis, upper airway infections, and sleep disturbances (e.g., snoring) take place. In addition, mouth breathing is often associated with a decrease in oxygen intake into the lungs. Mouth breathing can particularly affect the growing face, as the abnormal pull of these muscle groups on facial bones slowly deforms these bones, causing misalignment. The earlier in life these changes take place, the greater the alterations in facial growth, and ultimately an open mouth posture is created where the upper lip is raised and the lower jaw is maintained in an open posture. The tongue, which is normally tucked under the roof of the mouth, drops to the floor of the mouth and protrudes to allow a greater volume of air intake. Consequently, an open mouth posture can lead to malocclusions and problems in swallowing. Other causes of open-mouth posture are weakness of lip muscles, overall lack of tone in the body or hypotonia, and prolonged/chronic allergies of the respiratory tract. A.union

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.

A maxillary torus is only removed in instances where it is problematic. This includes cases where in an edentulous patient, it extends to the vibrating line, preventing a posterior seal of the denture and posterior seal at the fovea palatinae. Other indications for removal include frequent trauma to the torus, owing to its size or the thinness of the mucoperiosteum overlying it, disturbance of speech, and rapid growth in patients who are cancer-phobic.

Orofacial myofunctional disorders (OMD) (sometimes called “oral myofunctional disorder", and “tongue thrust”) are muscle disorders of the face, mouth, lips, or jaw.

Recent studies on incidence and prevalence of tongue thrust behaviors are not available. However, according to the previous research, 38% of various populations have OMD. The incidence is as high as 81% in children exhibiting speech/articulation problems (Kellum, 1992).

All cases reported appear to represent sporadic occurrence. There is no specific inheritance pattern. The male-to-female ratio of affected is 1.8:1 and is often diagnosed before the age of 9. The disorder affects the right and left sides of the maxilla almost equally.

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.

Torus palatinus "(pl. tori palatini)" [palatinus torus "(pl. palatal tori)" in English] is a bony protrusion on the palate. Palatal tori are usually present on the midline of the hard palate. Most palatal tori are less than 2 cm in diameter, but their size can change throughout life.

Prevalence of palatal tori ranges from 9–60% and are more common than bony growths occurring on the mandible, known as torus mandibularis. Palatal tori are more common in Asian, Native American and Inuit populations, and twice more common in females. In the United States, the prevalence is 20% - 35% of the population with similar findings between black and white people.

Although some research suggest palatal tori to be an autosomal dominant trait, it is generally believed that palatal tori are caused by several factors. They are more common in early adult life and can increase in size. In some older people, the size of the tori may decrease due to bone resorption. It is believed that tori of the lower jaw are the result of local stresses and not solely on genetic influences.

Sometimes, the tori are categorized by their appearance. Arising as a broad base and a smooth surface, flat tori are located on the midline of the palate and extend symmetrically to either side. Spindle tori have a ridge located at their midline. Nodular tori have multiple bony growths that each have their own base. Lobular tori have multiple bony growths with a common base.

Palatal tori are usually a clinical finding with no treatment necessary. It is possible for ulcers to form on the area of the tori due to repeated trauma. Also, the tori may complicate the fabrication of dentures. If removal of the tori is needed, surgery can be done to reduce the amount of bone present.