In dentistry, a furcation defect is bone loss, usually a result of periodontal disease, affecting the base of the root trunk of a tooth where two or more roots meet ("bifurcation" or "trifurcation"). The extent and configuration of the defect are factors in both diagnosis and treatment planning.

A tooth with a furcation defect typically possessed a more diminished prognosis owing to the difficulty of rendering the furcation area free from periodontal pathogens. For this reason, surgical periodontal treatment may be considered to either close the furcation defect with grafting procedures or allow greater access to the furcation defect for improved oral hygiene.

Taurodontism is a condition found in the molar teeth of humans whereby the body of the tooth and pulp chamber is enlarged vertically at the expense of the roots. As a result, the floor of the pulp and the furcation of the tooth is moved apically down the root. The underlying mechanism

of taurodontism is the failure or late invagination of Hertwig's epithelial root sheath, which is responsible for root formation and shaping causing an apical shift of the root furcation.

The constriction at the amelocemental junction is usually reduced or absent. Taurodontism is most commonly found in permanent dentition although the term is traditionally applied to molar teeth.

In some cases taurodontism seems to follow an autosomal dominant type of inheritance.

Taurodontism is found in association with amelogenesis imperfecta, ectodermal dysplasia and tricho-dento-osseous syndrome.

The term means "bull like" teeth derived from similarity of these teeth to those of ungulate or cud-chewing animals.

According to Shaw these can be classified as hypotaurodont, hypertaurodont and mesotaurodont.

According to Mangion taurodontism may be:

- A (mentally retarded) character

- A primitive pattern

- Mendelian recessive character

- Atavistic feature

- A mutation

It has also been reported in Klinefelter's syndrome, XXYY and Down's syndrome .

The teeth involved are invariably molars, sometimes single and at the other times multiple teeth may be involved. The teeth themselves may look normal and do not have any particular anatomical character on clinical examination.

On a dental radiograph, the involved tooth looks rectangular in shape without apical taper. The pulp chamber is extremely large and the furcations may be only a few millimeters long at times.

An enamel pearl is a condition of teeth where enamel is found in locations where enamel is not supposed to be, such as on a root surface. They are usually found in the area between roots, which is called a furcation, of molars. Enamel pearls are not common in teeth with a single root. The most common location of enamel pearls is the furcation areas of the maxillary and mandibular third molar roots.

Enamel pearls are formed from the Hertwig's Epithelial root sheath. After the initiation of the formation of dentin in the root area of the tooth, the root sheath disintegrates and moves away from the root surface so that the cells of the dental sac can come in contact with predentin to differentiate into cementoblasts and start deposition of cementum. However, if the cells of epithelial root sheath remain adherent to predentin, they may differentiate into fully functional ameloblasts and deposit enamel. Such droplets of enamel are called enamel pearls.

Nabers probe is used to check for furcation involvement clinically. Recently, cone beam computerised technology (CBCT) has also be used to detect furcation. Periapical and interproximal intraoral radiographs can help diagnosing and locating the furcation. The location and severity of furcation should be recorded in patient’s notes.

Only multirooted teeth have furcation. Therefore, upper first premolar, maxillary and mandibular molars may be involved.

Upper premolars have one buccal and one palatal root. Furcation involvement should be checked from the mesial and the distal aspects of the tooth.

Maxillary molars have three roots, a mesio-buccal root, disto-buccal root and a palatal root. Thus, check for furcation from buccal, mesio-palatal and disto-palatal aspects.

Mandibular molars have one mesial and one distal root, and so, check for involvement from buccal and lingual aspects.

Hair abnormalities are very prominent in majority of the cases of TDO. Kinky/curly hair that is unusually dry and easily sheds is present at birth. In 80% of cases, the hair has a more relaxed appearance by adolescence. The presence of this hair texture type is a defining characteristic between a diagnosis of TDO verses amelogenesis imperfecta with hypomaturation. Additionally, in TDO the nails are usually abnormally thin, brittle, and split frequently. Cranial deficiencies are marked by the presence of having a long skull relative to its width, or protrusive foreheads due to increased thickness of the cranial bones and premature closing of the associated sutures in the skull. The long bones in the body (arms, legs) are also abnormally long and tend to fracture very easily. Osteosclerosis, commonly seen in TDO cases is characterized by an increase in bone density, affecting the skull and the mastoid process located behind the jawbone on the skull, as well as a shortened ramus seen in people with TDO. There are no known pathological problems associated with hair and bone changes in people with this disease. Changes in the long bones tend to appear later in development, but changes in the teeth appear once the teeth being to form, called primary dentition. The hair and bone abnormalities are evaluated radiographically during initial diagnosis, and visually during the course of the disease. Radiographic exams may be repeated if there is suspect of fracture.

In the oral cavity 100% of people diagnosed with TDO have taurodontism which is characterized by vertically enlarged pulp chambers at the expense of the roots of the teeth; the floor of the pulp chamber and furcation is moved apically down. This is due to the failure of the Hertwig epithelial root sheath which maps the shape of the forming tooth roots during active differentiation. Amelogenesis imperfecta, an abnormal formation of the enamel or external layer of the crown of the tooth, may also be present where the tooth enamel may be thin or absent. There are several clinical subsets of amelogenesis imperfecta, but common to TDO is the hypoplastic-hypomaturation subtype; the hypomaturation-hypoplastic is less common in individuals with TDO. The difference between the 2 dominant subtypes is the changes seen in the enamel matrix, and the phenotypic type that predominates. The hypoplastic-hypomaturation type of amelogenesis imperfecta with TDO occurs where the tooth enamel depicts a generalized pitted pattern, with open contacts between the teeth as well as an open bite. A smaller amount of cases are of the hypomaturation-hypoplastic case type, in which the enamel structure is softer due to the under maturation of ameloblasts during development. Mandibular prognathism also called a severe underbite, is also a prominent feature in TDO. Prognathism defects are diagnosed based the level of severity that this condition interferes with being able to chew or speak properly.

Due to improper tooth development, TDO patients suffer from high rates of dental caries causing dental abscess. The under maturation of the enamel causes the tooth structure to be softer, and more susceptible to the effects of bruxism due to abnormalities in skeletal development. The oral abnormalities are evaluated by radiographs and visual examination. Oral radiographs are frequently repeated due to the high incidence of infection due to abnormal biting patterns seen in TDO cases.

Clinical examination and x rays can help diagnose the condition. For examples :

- Valsalva test (nose blowing test): Ask the patient to pinch the nostrils together and open the mouth, then blow gently through the nose. Observe if there is passage of air or bubbling of blood in the post extraction alveolus as the trapped air from closed nostrils is forced into the mouth through any oroantral communication. Gentle suction applied to the socket often produces a characteristic hollow sound.

- Perform a complete extra- and intra-oral examination using a dental mirror under good lighting, look for granulation tissue in the socket and openings into the antrum.

- Panoramic radiograph or paranasal computed tomography can help to locate the fistula, the size of it and to determine the presence of sinusitis and other foreign bodies. Other methods like radiographs (occipitomental, OPG and periapical views) can also be used to confirm the presence of any oroantral fistulas.

- To test the patency of communication the patient is asked to rinse the mouth or water is flushed in the tooth socket.

- Unilateral epistaxis is seen in case of collection of blood in the sinus cavity.

- Do not probe or irrigate the site, because it may lead to sinusitis or push foreign bodies, such as contaminated fragments, or oral flora further into the antrum. Hence, leading to the formation of a new fistula or widen an existing one.

The maxillary sinus is known for its thin floor walls and close proximity to the posterior maxillary teeth. Dental procedures such as extraction of these teeth sometimes cause OAC. The posterior maxillary molars and maxillary sinus are innervated by the same branch of nerves which is the maxillary division of trigeminal nerve. This innervation complicates the situation as the pain from maxillary sinus might be indistinguishable from a posterior maxillary toothache. Other known causes of OAC are fracture across the antral floor typically Le Fort I, displacement of posterior maxillary molar roots into antrum, and direct trauma. Extraction of primary teeth are not considered a risk of OAC due to the presence of developing permanent teeth and the small size of a developing maxillary sinus. OAC can happen for many other reasons, such as acute or chronic inflammatory lesions around the apex of tooth root present in close proximity with the maxillary antrum, necrotic lesions of the maxilla, failure of sublabial incision to heal after Caldwell-luc antrostomy, multiple and extensive fractures of the facial region, Osteomyelitis of the maxilla, injudicious use of instruments during oral procedures, malignancy of the maxillary sinus, Syphilis, malignant granuloma, radiotherapy, implant denture, removal of a large cyst or resection of large tumour involving maxilla, development of tumour causing bone destruction and loosening of teeth.

Chronic periodontitis is a common disease of the oral cavity consisting of chronic inflammation of the periodontal tissues that is caused by accumulation of profuse amounts of dental plaque, that may or may not be caused genetically.

There are four types of abscesses that can involve the periodontal tissues:

1. Gingival abscess—a localized, purulent infection involves only the soft gum tissue near the marginal gingiva or the interdental papilla.

2. Periodontal abscess—a localized, purulent infection involving a greater dimension of the gum tissue, extending apically and adjacent to a periodontal pocket.

3. Pericoronal abscess—a localized, purulent infection within the gum tissue surrounding the crown of a partially or fully erupted tooth. Usually associated with an acute episode of pericoronitis around a partially erupted and impacted mandibular third molar (lower wisdom tooth).

4. combined periodontal/endodontic abscess

It is one of the seven destructive periodontal diseases as listed in the 1999 classification.

A periodontal abscess (also termed lateral abscess, or parietal abscess), is a localized collection of pus (i.e. an abscess) within the tissues of the periodontium. It is a type of dental abscess. A periodontal abscess occurs alongside a tooth, and is different from the more common periapical abscess, which represents the spread of infection from a dead tooth (i.e. which has undergone pulpal necrosis). To reflect this, sometimes the term "lateral (periodontal) abscess" is used. In contrast to a periapical abscess, periodontal abscesses are usually associated with a vital (living) tooth. Abscesses of the periodontium are acute bacterial infections classified primarily by location.

There are no symptoms, and no signs can be elicited on examination. Medical imaging such as traditional radiography or computed tomography is required to demonstrate the defect. Usually the defect is unilateral, but occasionally can be bilateral.

It is a classed as a pseudocyst, since there is no epithelial lining or fluid content. This defect is usually considered with other cysts of the jaws, since it can be mistaken for such on a radiograph.

Osteoporotic bone marrow defect is a condition which may be found in the body of the mandible. It is usually painless and found during routine radiographs. It appears as a poorly defined radiolucency (dark area) where there was a previous history of an extraction of a tooth. It may resemble a metastatic disease.

It is a localized increase of hematopoietic bone marrow that creates a radiolucent radiographic defect. They occur more commonly in women in the midyears and show a predilection for the molar region of the mandible. They are especially common in extraction sites. Scattered trabeculae may extend short distances into the defect or, in some instances, through it, giving the defect a fairly characteristic appearance. Naturally there are no clinical symptoms.

This defect may easily be mistaken for a cyst or tumor. Biopsy is required to rule these out.

The condition is of anthropological importance as it was seen in Neanderthals.

The trait ""is common among extant New World monkeys, apes, and fossil hominins"".

The tibia is the most commonly involved bone, accounting for 85% of cases. It is usually painless, although there may be localized pain or fracture, and presents as a localized firm swelling of the tibia in children less than two decades old (median age for males 10, females 13). Several authors have related this non-neoplastic lesion to adamantinoma - a tumor involving subcutaneous long bones - stating the common cause to be fibrovascular defect. However, the latter is distinguished from an osteofibrous dysplasia by the presence of soft tissue extension, intramedullary extension, periosteal reaction and presence of hyperchromic epithelial cells under the microscope.

Osteofibrous dysplasia may also be mistaken for fibrous dysplasia of bone, although osteofibrous dysplasia is more likely to show an immunohistochemical reaction to osteonectin, neurofibromin, and S-100 protein.

Cleidocranial dysostosis is a general skeletal condition so named from the collarbone (cleido-) and cranium deformities which people with it often have.

People with the condition usually present with a painless swelling in the area of the clavicles at 2–3 years of age. Common features are:

- Clavicles (collarbones) can be partly missing leaving only the medial part of the bone. In 10% cases, they are completely missing. If the collarbones are completely missing or reduced to small vestiges, this allows hypermobility of the shoulders including ability to touch the shoulders together in front of the chest. The defect is bilateral 80% of the time. Partial collarbones may cause nerve damage symptoms and therefore have to be removed by surgery.

- The mandible is prognathic due to hypoplasia of maxilla (micrognathism) and other facial bones.

- A soft spot or larger soft area in the top of the head where the fontanelle failed to close, or the fontanelle closes late.

- Bones and joints are underdeveloped. People are shorter and their frames are smaller than their siblings who do not have the condition.

- The permanent teeth include supernumerary teeth. Unless these supernumeraries are removed they will crowd the adult teeth in what already may be an underdeveloped jaw. If so, the supernumeraries will probably need to be removed to make space for the adult teeth. Up to 13 supernumarary teeth have been observed. Teeth may also be displaced. Cementum formation may be deficient.

- Failure of eruption of permanent teeth.

- Bossing (bulging) of the forehead.

- Open skull sutures, large fontanelles.

- Hypertelorism.

- Delayed ossification of bones forming symphysis pubis, producing a widened symphysis.

- Coxa vara can occur, limiting abduction and causing Trendelenburg gait.

- Short middle fifth phalanges, sometimes causing short and wide fingers.

- Vertebral abnormalities.

- On rare occasions, brachial plexus irritation can occur.

- Scoliosis, spina bifida and syringomyelia have also been described.

Other features are: parietal bossing, basilar invagination (atlantoaxial impaction), persistent metopic suture, abnormal ear structures with hearing loss, supernumerary ribs, hemivertebrae with spondylosis, small and high scapulae, hypoplasia of illiac bones, absence of the pubic bone, short / absent fibular bones, short / absent radial bones, hypoplastic terminal phalanges.

Osteofibrous dysplasia (also known as ossifying fibroma) is a rare, benign non-neoplastic condition with no known cause. It is considered a fibrovascular defect. Campanacci described this condition in two leg bones, the tibia and fibula, and coined the term. This condition should be differentiated from Nonossifying fibroma and fibrous dysplasia of bone.

Cleidocranial dysostosis (CCD), also called cleidocranial dysplasia, is a birth defect that mostly affects the bones and teeth. The collarbones are typically either poorly developed or absent, which allows the shoulders to be brought close together. The front of the skull often does not close until later, and those affected are often shorter than average. Other symptoms may include a prominent forehead, wide set eyes, abnormal teeth, and a flat nose. Symptoms vary among people; however, intelligence is typically normal.

The condition is either inherited from a person's parents or occurs as a new mutation. It is inherited in an autosomal dominant manner. It is due to a defect in the RUNX2 gene which is involved in bone formation. Diagnosis is suspected based on symptoms and X-rays with confirmation by genetic testing. Other conditions that can produce similar symptoms include mandibuloacral dysplasia, pyknodysostosis, osteogenesis imperfecta, and Hajdu-Cheney syndrome.

Treatment includes supportive measures such as a device to protect the skull and dental care. Surgery may be performed to fix certain bone abnormalities. Life expectancy is generally normal.

It affects about one per million people. Males and females are equally commonly affected. Modern descriptions of the condition date to at least 1896. The term is from "cleido" meaning collarbone, "cranial" meaning head, and "dysostosis" meaning formation of abnormal bone.

Blau Syndrome is an autosomal dominant genetic inflammatory disorder which affects the skin, eyes, and joints. It is caused by a mutation in the NOD2 (CARD15) gene. Symptoms usually begin before the age of 4, and the disease manifests as early onset cutaneous sarcoidosis, granulomatous arthritis, and uveitis.

Mirizzi's syndrome has no consistent or unique clinical features that distinguish it from other more common forms of obstructive jaundice. Symptoms of recurrent cholangitis, jaundice, right upper quadrant pain, and elevated bilirubin and alkaline phosphatase may or may not be present. Acute presentations of the syndrome include symptoms consistent with cholecystitis.

Surgery is extremely difficult as Calot's triangle is often completely obliterated and the risks of causing injury to the CBD are high.

Tracheal agenesis is a rare birth defect with a prevalence of less than 1 in 50,000, in which the trachea fails to develop. The defect is normally fatal, although occasional cases have been reported of long-term survival following surgical intervention.

There are three main types of tracheal agenesis, designated Types I, II and III.

In 2013, a case was reported of a South Korean child with tracheal agenesis who had been successfully treated after having been kept alive in an intensive care unit for the first two and a half years of her life. She then had an artificially created trachea implanted that had been created by tissue engineering using her own stem cells. The patient however later died from complications.

Osteoporosis is due to causal factors like atrophy of disuse and gonadal deficiency. Hence osteoporosis is common in post menopausal women and in men above 50 yrs. Hypercorticism may also be causal factor, as osteoporosis may be seen as a feature of Cushing's syndrome.