There is only very weak evidence linking to coronary heart disease.

There is little evidence linking progression of periodontal disease to low birth weight or preterm birth:

"In these women with periodontitis and within this study's limitations, disease progression was not associated with an increased risk for delivering a pre-term or a low birthweight infant."

There is recently emerged evidence linking chronic periodontitis with head and neck squamous cell carcinoma: "Patients with periodontitis were more likely to have poorly differentiated oral cavity SCC than those without periodontitis (32.8% versus 11.5%; P = 0.038)".

There is evidence to suggest that periodontal disease may play a role in the pathogenesis of Alzheimer's Disease.

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.

OAF is a complication of oroantral communication. Other complications may arise if left untreated. For example:

- Candidal infection

- Chronic maxillary sinus infection of bacterial origin

- Osteomyelitis

- Rhinosinusitis

- Sinus pathology

Therefore, OAF should be dealt with first, before treating the complications.

Studies have shown that sinusitis is found in about 60% of the cases on the fourth day after the manifestation of sinus. Moreover, patient may be afflicted with an acute sinus disease if OAC is not treated promptly upon detecting clear signs of sinusitis. So, early diagnosis of OAC must be conducted in order to prevent OAF from setting in.

Spontaneous healing of small perforation is expected to begin about 48 hours after tooth extraction and it remains possible during the following two weeks. Patient must consult the dentist as early as possible should a large defect of more than 7mm in diameter or a dogged opening that requires closure is discovered so that appropriate and suitable treatment can be swiftly arranged or referral to Oral Maxillofacial Surgery (OMFS) be made at the local hospital, if required.

A comprehensive preoperative radiographic evaluation is a must as the risk of OAC can increase due to one or more of the following situations :-

- Close relationship between the roots of the maxillary posterior teeth and the sinus floor

- Increased divergence or dilaceration of the roots of the tooth

- Marked pneumatization of the sinus leading to a larger size

- Peri-radicular lesions involving teeth or roots in close association with the sinus floor

Hence, in such cases:

- Avoid using too much of apical pressure during tooth extraction

- Perform surgical extraction with roots sectioning

- Consider referral to OMFS at local hospital

The treatment aims are to eliminate the bacteria from the exposed surface of the root(s) and to establish the anatomy of the tooth, so that better plaque control can be achieved. Treatment plans for patients differ depending on the local and anatomical factors.

For Grade I furcation, scaling and polishing, root surface debridement or furcationplasty could be done if suitable.

For Grade II furcation, furcationplasty, open debridement, tunnel preparation, root resection, extraction, guided tissue regeneration (GTR) or enamel matrix derivative could be considered.

As for Grade III furcation, open debridement, tunnel preparation, root resection, GTR or tooth extraction could be performed if appropriate.

Tooth extraction is usually considered if there is extensive loss of attachment or if other treatments will not obtain good result (i.e. achieving a nice gingival contour to allow good plaque control).

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.

Amelogenesis imperfecta hypomaturation type with taurodontism are often confused. Amelogenesis imperfecta of the hypomaturation type with taurodontism (AIHHT) has no hair or bone changes which helps to differentiate between TDO cases and AIHHT. Polymerase chain reaction also known as PCR is used to amply pieces of DNA and observed for the 141 base pair allele as a result of a deletion of four nucleotides in exon 3 of the DLX-3 gene. Additionally, the current research shows that there is heavy reliance on the physical characteristics in the differentiation of TDO verses AIHHT and the severity and prevalence of their expression. For instance, taurodontism is severely expressed in TDO, but mildly expressed in AIHHT. Currently, researchers are trying to identify the reason for the alteration in the DLX-3 and DLX-7 genes that are responsible for AIHHT versus TDO.

A single copy of the abnormal gene from one parent is able to cause the disease; this is called autosomal dominance. A mutation in the DLX3 gene has been confirmed as the cause of TDO. The onset of TDO begins with a 4 base pair deletion on chromosome 17q21, causing a mutation, specifically frameshift, and the termination codon to be the cause of the lack of complete maturation of the tooth enamel; this mutation is also responsible for the osseous defects in the bone. DLX-3 is expressed in the placenta and is significantly important during embryonic development in regards to hard bone tissue which is present in the teeth, skull, and long bones such as in the arms and legs. During normal tooth development, DLX 3 shifts from predominant expression in the inner enamel epithelium; the outer layer does not express DLX 3. In TDO cases, the DLX-3 is present on the outer enamel epithelium and leads to the dental abnormalities seen in this disease. Improper expression of DLX-3 causes the tooth enamel to be thinner, which leads to attrition and is most often the cause of dental abscess seen in TDO persons.

During osseous, connective tissue, and dermal cell differentiation, DLX 3 in TDO is also responsible for upper cranial thickness, calvaria, osteosclerosis of the long bones, long narrow head (dolichocephaly), abnormally thin brittle nails, and premature closing of fibrous joints. Consequently, 95% of people with TDO that are 16 years old or younger show skeletal abnormalities before full maturation takes place. Lack of mastoid pneumatization by mastoid cells occurs in 82% of the cases and is rarely prevalent outside of TDO diagnosis. Mastoid pneumatization occurs at about 6 months of ages and acts to minimize pressure fluctuations in the Eustachian tubes of the ear. The mastoid lies posterior to the lower jawbone (mandible) and distal to the ear. The Eustachian tube connects the middle ear to the back of the nose, and acts to create a specific pressure in the ear canal that causes vibrations to the eardrum; if adequate pressure is not attained, muffled, dull hearing results. In addition to the mastoid pneumatization assisting the Eustachian tubes for normal hearing, lack of mastoid pneumatization causes inflammation of the ear, general irritation, and does not allow enough air in to assist with mucus flowing out. It is not completely understood why gene mutations occur, but it is known that genetic mutations that cause disease are acquired from either or both parents at fertilization.

Stafne defect is uncommon, and has been reported to develop anywhere between the ages of 11 and 30 years old, (although the defect is developmental, it does not seem to be present form birth, implying that the lesion develops at a later age). Usually the defect is unilateral (on one side only) and most commonly occurs in men.

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.

A periodontal abscess most commonly occurs as a complication of advanced periodontal disease (which is normally painless). A periodontal pocket contains dental plaque, bacteria and subgingival calculus. Periodontal pathogens continually find their way into the soft tissues, but normally they are held in check by the immune system. A periodontal abscess represents a change in this balance, related to decreased local or systemic resistance of the host. An inflammatory response occurs when bacteria invade and multiply within the soft tissue of the gingival crevice/periodontal pocket. A pus-filled abscess forms when the immune system responds and attempts to isolate the infection from spreading.

Communication with the oral environment is maintained via the opening of the periodontal pocket. However, if the opening of a periodontal pocket becomes obstructed, as may occur if the pocket has become very deep (e.g. with furcation involvement), then plaque and calculus are trapped inside. Food packing may also obstruct a periodontal pocket. Food packing is usually caused by failure to accurately reproduce the contact points when dental restorations are placed on the interproximal surfaces of teeth. Another potential cause occurs when a periodontal pocket is scaled incompletely. Following this procedure, the gingival cuff tightens around the tooth, which may be enough to trap the bacteria left in the pocket. A gingival retraction cord which is accidentally left "in situ" is an occasional cause of a periodontal abscess.

Penetrating injury to the gingiva e.g. with a toothbrush bristle, fishbone, toothpick or periodontal instrument may inoculate bacteria into the tissues. Trauma to the tissues, e.g. caused by an impact on a tooth, or excessive pressure exerted on teeth during orthodontic treatment. Occlusal overload may also be involved in the development of a periodontal abscess, but this is rare and usually in combination with other factors. Bruxism is a common cause of excessive occlusal forces.

Systemic immune factors such as diabetes can predispose to the formation of periodontal abscesses.

Perforation of a root canal during endodontic therapy can also lead to a periodontal abscess.

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.

The Stafne defect is thought to be caused by an ectopic portion of the submandibular salivary gland which causes the bone of the lingual cortical plate to remodel. Rarely, the defect can be completely surrounded by bone, and this has been theorized to be the result of entrapment of embyonic salivary gland tissue within the bone. Similar, but rarer, defects may be present in the anterior portion of the lingual surface of the mandible. These are not termed Stafne defects which specifically refers to the posterior location. The anterior defects may be associated with the sublingual salivary gland.

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"".

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.

Osteofibrous dysplasia is treated with marginal resection with or without bone grafting, depending on the size of the lesion and the extent of bony involvement. However, due to the high rate of recurrence in skeletally immature individuals, this procedure is usually postponed until skeletal maturity.

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.

Several studies have reported that life expectancy appears to be normal for people with CCD.

It is usually autosomal dominant, but in some cases the cause is not known. It occurs due to haploinsufficiency caused by mutations in the CBFA1 gene (also called Runx2), located on the short arm of chromosome 6, which encodes transcription factor required for osteoblast differentiation. It results in delayed ossification of midline structures of the body, particularly membranous bone.

A new article reports that the CCD cause is thought to be due to a CBFA1 (core binding factor activity 1) gene defect on the short arm of chromosome 6p21 . CBFA1 is vital for differentiation of stem cells into osteoblasts, so any defect in this gene will cause defects in membranous and endochondral bone formation.

Risk factors for developing a cystocele are:

- an occupation involving or history of heavy lifting

- pregnancy and childbirth

- chronic lung disease/smoking

- family history of cystocele

- exercising incorrectly

- ethnicity (risk is greater for Hispanic and whites)

- hypoestrogenism

- pelvic floor trauma

- connective tissue disorders

- spina bifida

- hysterectomy

- cancer treatment of pelvic organs* childbirth; correlates to the number of births

- forceps delivery

- age

- chronically high intra-abdominal pressures

- chronic obstructive pulmonary disease

- constipation

- obesity

Connective tissue disorders predispose women to developing cystocele and other pelvic organ prolapse. The tensile strength of the vaginal wall decreases when the structure of the collagen fibers change and become weaker.

Though articular cartilage damage is not life-threatening, it does strongly affect one's quality of life. Articular cartilage damage is often the cause of severe pain, knee swelling, substantial reduction in mobility and severe restrictions to one's activities. Over the last decades, however, research has focused on regenerating damaged joints.

These regenerative procedures are believed to delay osteoarthritis of injuries on the articular cartilage of the knee, by slowing down the degeneration of the joint compared to untreated damage. According to Mithoefer "et al." (2006), these articular cartilage repair procedures offer the best results when the intervention takes place in the early stages of the cartilage damage.

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.

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.