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.

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.

Oroantral fistula (OAF) is an abnormal condition of the face where the maxillary sinus is exposed to the oral cavity through an epithelialised fistula. This term signifies pathology and it is not to be confused with oroantral communication (OAC). OAC if left untreated can either heal spontaneously or progress into OAF. The fistulous opening may be situated on the alveolus.

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.

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.

The Stafne defect (also termed Stafne's idiopathic bone cavity, Stafne bone cavity, Stafne bone cyst (misnomer), lingual mandibular salivary gland depression, lingual mandibular cortical defect, latent bone cyst, or static bone cyst) is a depression of the mandible on the lingual surface (the side nearest the tongue). The Stafne defect is thought to be a normal anatomical variant, as the depression is created by ectopic salivary gland tissue associated with the submandibular gland and does not represent a pathologic lesion as such.

Since alveolar osteitis is not primarily an infection, there is not usually any pyrexia (fever) and cervical lymphadenitis (swollen glands in the neck), and only minimal edema (swelling) and erythema (redness) is present in the soft tissues surrounding the socket.

Signs may include:

- An empty socket, which is partially or totally devoid of blood clot. Exposed bone may be visible or the socket may be filled with food debris which reveals the exposed bone once it is removed. The exposed bone is extremely painful and sensitive to touch. Surrounding inflamed soft tissues may overlie the socket and hide the dry socket from casual examination.

- Denuded (bare) bone walls.

Symptoms may include:

- Dull, aching, throbbing pain in the area of the socket, which is moderate to severe and may radiate to other parts of the head such as the ear, eye, temple and neck. The pain normally starts on the second to fourth day after the extraction, and may last 10–40 days. The pain may be so strong that even strong analgesics do not relieve it.

- Intraoral halitosis (oral malodor).

- Bad taste in the mouth.

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.

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.

The characteristic symptom of Degos disease is the development of papules. Initially, individuals may have skin lesions or rashes, but they will proceed to develop distinct bumps, or papules. Papules are circular in shape, have a porcelain-white center and red border. As papules age, the white centers will skin in and only the border will remain raised. Typically, papules range from 0.5 to 1 cm in width. Papules appear on the trunk and upper extremities and are not found on the individual's palms, soles, scalp, or face.

Depending on whether an individual has the benign variant or malignant variant of the disease symptoms will vary. Both the benign and malignant forms have development of the characteristic papules. Individuals with the benign form will have the typical papules persisting anywhere from a few years to throughout their whole lives. In the benign form, no inner organs are affected. If an individual develops the malignant form, it means that not only are the papules present, but inner organs are involved. Most malignant cases involve problems of the gastrointestinal tract leading to small intestine lesions, abdominal pain, diarrhea, and bowel perforation. If the central nervous system is involved, symptoms can include headaches, dizziness, seizures, paralysis of cranial nerves, weakness, stroke, damage to small areas of the brain due to artery blockage (cerebral infarcts, and cerebral hemorrhage). Additional organs commonly impacted include the heart, lungs, and kidneys. Symptoms that may develop from damage to these organs include double vision (diploplia), clouding of lenses of eyes, swelling of the optic disc (papilledema), partial loss of vision, shortness of breath, chest pain, epilepsy,and thickening of pericardium.

Someone with the benign form may suddenly develop symptoms of the malignant form. Symptoms can last anywhere from a few weeks to several years. Onset of symptoms typically begins to manifest between the ages of 20-50. A few cases of this condition in newborns have also been described.

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.

Fetal trimethadione syndrome is characterized by the following major symptoms as a result of the teratogenic characteristics of trimethadione.

- Cranial and facial abnormalities which include; microcephaly, midfacial flattening, V-shaped eyebrows and a short nose

- Cardiovascular abnormalities

- Absent kidney and ureter

- Meningocele, a birth defect of the spine

- Omphalocele, a birth defect where portions of the abdominal contents project into the umbilical cord

- A in mental and physical development

Since dry socket occurs exclusively following a dental extraction, it could be considered both a complication and an iatrogenic condition, but this does not take into account both the reason why the tooth required extraction (i.e., extraction may have been unavoidable due to significant pain and infection) and also the fact that many dry sockets are the result of poor compliance with postoperative instructions, notably refraining from smoking in the days immediately after the procedure.

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

Clinical evaluation and identification of characteristics papules may allow a dermatologist to diagnose Degos disease. The papules have a white center and are bordered with a red ring. After lesions begin to appear, the diagnosis for Degos disease can be supported by histological findings. Most cases will show a wedge-shaped connective tissue necoris in the deep corium. This shape is due to the blockage/occlusion of small arteries.

Individuals may be diagnosed with the benign form if only the papules are present. However, an individual may be diagnosed with the malignant form if involvement of other organs like the lungs, intestine and/or central nervous system occurs. The malignant, or systematic form of this condition may suddenly develop even after having papules present for several years. In order to quickly diagnose this shift to the malignant variant of the disease, it is important for individuals to have consistent follow-up evaluations.In these evaluations, depending on which organs are suspected to be involved, the following procedures and tests may be conducted: skin inspection, brain magnetic resonance tomography, colonoscopy, chest X-ray, and/or abdominal ultrasound.

The mean age at presentation is thirty-seven years with a reported range of nineteen to sixty-four years. The mean age of onset since diagnosis of diabetes is fifteen years. The female:male ratio is 1.3:1. Other diabetic complications such as nephropathy, neuropathy, retinopathy and hypertension are usually present. Its major symptom is the acute onset muscle pain, usually in the thigh, in the absence of trauma. Signs include exquisite muscle tenderness and swelling.

Pain may be the first noticed symptom. People with lipodermatosclerosis have tapering of their legs above the ankles, forming a constricting band resembling an inverted champagne bottle. In addition, there may be brownish-red pigmentation and induration.

Microcoria is a congenital disease in which the pupils of the subject are narrower than 2 mm in diameter. Microcoria is associated with juvenile-onset glaucoma. It is also associated with Pierson syndrome chararacterized by microcoria and congenital nephrotic syndrome. The defect is in the Laminin beta 2 gene on chromosome 3p21 which encodes a protein essential to the glomerular basement membrane.

It is also part of the known manifestations of a born infant to a mother suffering from uncontrolled hyperglycemia. Other symptoms include transposition of great vessels, respiratory distress secondary to surfactant defect, sacral agensis, jitteriness, irritability, and lethargy due to rebound fetal hypoglycemia. Congenital microcoria is an autosomal dominant trait. However, it can also occur sporadically.

Fetal trimethadione syndrome (also known as paramethadione syndrome, German syndrome, tridione syndrome, among others) is a set of birth defects caused by the administration of the anticonvulsants trimethadione (also known as Tridione) or paramethadione to epileptic mothers during pregnancy.

Fetal trimethadione syndrome is classified as a rare disease by the National Institute of Health's Office of Rare Diseases, meaning it affects less than 200,000 individuals in the United States.

The fetal loss rate while using trimethadione has been reported to be as high as 87%.

Individuals with QPD are at risk for experiencing a number of bleeding symptoms, including joint bleeds, hematuria, and large bruising. In 2010, the genetic cause of QPD has been determined as a mutation involving an extra copy of the uPA (urokinase plasminogen activator) gene http://bloodjournal.hematologylibrary.org/content/115/6/1264.long. The mutation causes overproduction of an enzyme that accelerates blood clot breakdown.

Diabetic myonecrosis is a complication of diabetes. It is caused by infarcted muscle tissue, usually in the thigh.

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.

Brunner syndrome is a rare genetic disorder associated with a mutation in the MAOA gene. It is characterized by lower than average IQ (typically about 85), problematic impulsive behavior (such as arson, hypersexuality and violence), sleep disorders and mood swings. It was identified in fourteen males from one family in 1993. It has since been discovered in two additional families.

The syndrome has five characteristic findings:

- Omphalocele

- Anterior diaphragmatic hernia

- Sternal cleft with or without ectopia cordis

- Diaphragmatic pericardium defects (no diaphragmatic pericardium)

- Intracardiac defect: ventricular septal defect, diverticulum of the left ventricle, Tetralogy of Fallot

The discovery was found by a team of doctors at McMaster University, led by Dr. Catherine Hayward, a hematologist.