This type of gingival enlargement is sometimes termed "drug induced gingival enlargement" or "drug influenced gingival enlargement", abbreviated to "DIGO". Gingival enlargement may also be associated with the administration of three different classes of drugs, all producing a similar response: Gingival overgrowth is a common side effect of phenytoin, termed "Phenytoin-induced gingival overgrowth" (PIGO).

- anticonvulsants (such as phenytoin, phenobarbital, lamotrigine, vigabatrin, ethosuximide, topiramate and primidone NOT common for valproate)

- calcium channel blockers (antihypertensives such as nifedipine, amlodipine, and verapamil). The dihydropyridine derivative isradipidine can replace nifedipine and does not induce gingival overgrowth.

- cyclosporine, an immunosuppresant.

Of all cases of DIGO, about 50% are attributed to phenytoin, 30% to cyclosporins and the remaining 10-20% to calcium channel blockers.

Drug-induced enlargement has been associated with a patient's genetic predisposition, and its association with inflammation is debated. Some investigators assert that underlying inflammation is necessary for the development of drug-induced enlargement, while others purport that the existing enlargement induced by the drug effect compounds plaque retention, thus furthering the tissue response. Careful attention to oral hygiene may reduce the severity of gingival hyperplasia. In most cases, discontinuing the culprit drug resolves the hyperplasia.

Many systemic diseases can develop oral manifestations that may include gingival enlargement, some that are related to conditions and others that are related to disease:

- Conditioned enlargement

- pregnancy

- puberty

- vitamin C deficiency

- nonspecific, such as a pyogenic granuloma

- Systemic disease causing enlargement

- leukemia

- granulolomatous diseases, such as granulomatosis with polyangiitis, sarcoidosis, or orofacial granulomatosis.

- neoplasm

- benign neoplasms, such as fibromas, papillomas and giant cell granulomas

- malignant neoplasms, such as a carcinoma or malignant melanoma

- false gingival enlargements, such as when there is an underlying bony or dental tissue lesion

This condition occurs in association with denture wearing, and so those affected tend to be middle aged or older adults. 66-75% are estimated to occur in women. Epulis fissuratum is the third most common reactive lesion that occurs in the mouth, after peripheral giant cell granuloma and pyogenic granuloma.

OFG is uncommon, but the incidence is increasing. The disease usually presents in adolescence or young adulthood. It may occur in either sex, but males are slightly more commonly affected.

If the causative factor persists, tissue will become more fibrous over time.

There are many possible causes of gingival bleeding. The main cause of gingival bleeding is the formation and accumulation of plaque at the gum line due to improper brushing and flossing of teeth. The hardened form of plaque is calculus. An advanced form of gingivitis as a result of formation of plaque is periodontitis. Other causes that can exacerbate gingival bleeding include:

- placement of new dentures

- tooth or gum infection

- diabetes mellitus

- idiopathic thrombocytopenic purpura

- leukemia

- malnutrition

- use of aspirin and anticoagulants(blood thinners) such as warfarin and heparin

- hormonal imbalances during puberty and pregnancy

- iron overload

Other less common causes are:

- vitamin C deficiency (scurvy) and vitamin K deficiency

- dengue fever

Smoking and tobacco use of any kind are associated with increased risk of dry socket. This may be partially due to the vasoconstrictive action of nicotine on small blood vessels. Abstaining from smoking in the days immediately following a dental extraction reduces the risk of a dry socket occurring.

Risk factors associated with gingivitis include the following:

- age

- osteoporosis

- low dental care utilization (fear, financial stresses, etc.)

- poor oral hygiene

- overly aggressive oral hygiene such as brushing with stiff bristles

- mouth-breathing during sleep

- medications that dry the mouth

- cigarette smoking

- genetic factors

- pre-existing conditions

Some researchers suggest that HGF is transmitted as a Mendelian trait since both autosomal dominant and autosomal recessive transmission has been reported since the early 1970s. (SOURCE 1) In more recent scientific literature, there is evidence in which pedigree analyses confirm autosomal dominant, autosomal recessive or even as X-linked inherited cases of the HGF trait.

In 2002, researchers described the SOS1 gene and proved for the first time that a single-nucleotide–insertion mutation of the SOS1 gene on codon 1083 is the preliminary cause of HGF1 in humans. (Source 1) Later on in 2010, there was a case study done on a 16-year-old male with severe gingival overgrowth, almost covering all teeth. Researchers approached this issue with periodontics - a partial gingivectomy and flap surgery. This case study concluded that surgery followed by regular follow-ups is a good way to treat HGF despite the fact that the risks of re-occurrence of the condition remain high.

Even more recently, a study was done in 2013 on a family that showed history of autosomal recessive inheritance of HGF. The study did not dismiss the return of HGF after treatment but did claim that general surgical intervention after scaling and root planning of teeth supplemented with good oral hygiene is good enough to prevent the re-occurrence of HGF. This case study also acknowledged how HGF can be part of a multi-system syndrome associated with disorders such as Zimmermann Laband syndrome (ear, nose, bone, and nail defects with hepatosplenomegaly), Rutherford syndrome (microphthalmia, mental retardation, athetosis, and hypopigmentation), Murray-Puretic Drescher syndrome and Ramon syndrome.

Periapical periodontitis of some form is a very common condition. The prevalence of periapical periodontitis is generally reported to vary according to age group, e.g. 33% in those aged 20–30, 40% in 30- to 40-year-olds, 48% in 40- to 50-year-olds, 57% in 50- to 60-year-olds and 62% in those over the age of 60. Most epidemiologic data has been generated in European countries, especially Scandinavia. Millions of root canal treatments are carried out in the United States each year, although the total number of root canal treatments is an imperfect indicator of the prevalence of periapical periodontitis, since not always is it performed due to the presence of periapacial periodontitis, and not all cases of asymptomatic periodontitis will be treated in this manner, either due to lack of patient attendance or watchful waiting.

Overall, the incidence of dry socket is about 0.5–5% for routine dental extractions, and about 25–30% for impacted mandibular third molars (wisdom teeth which are buried in the bone).

Females are more frequently affected than males, but this appears to be related to oral contraceptive use rather than any underlying gender predilection. The majority of dry sockets occur in individuals aged between 20 and 40 which is when most dental extractions occur, although for any given individual it is more likely to occur in with increasing age.

Other possible risk factors include periodontal disease, acute necrotizing ulcerative gingivitis, local bone disease, Paget's disease of bone, osteopetrosis, cemento-osseous dysplasia, a history of previously developing a dry socket with past extractions and inadequate oral hygiene. Other factors in the postoperative period that may lead to loss of the blood clot include forceful spitting, sucking through a straw, and coughing or sneezing.

There is no treatment, but because this is a benign condition with no serious clinical complications, prognosis is excellent.

The following can occur if left untreated:

- Too much gingiva exposure

- Oral morbidity

- Chronic infection of areas between the gums and teeth, or at the gum line

- various degrees of Periodontitis - most likely due to the inability and difficulty of keeping the gingival margin and surrounding tissue clean due to the overgrowth

- Improper tooth eruption and/or complete prevention of tooth eruption as a result of too much gingiva exposure

- Systemic every-day troubles including functional and aesthetic problems of the mouth

- Malocclusion

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.

Untreated, the infection may lead to rapid destruction of the periodontium and can spread, as necrotizing stomatitis or noma, into neighbouring tissues in the cheeks, lips or the bones of the jaw. As stated, the condition can occur and be especially dangerous in people with weakened immune systems. This progression to noma is possible in malnourished susceptible individuals, with severe disfigurement possible.

Lichen sclerosus may have a genetic component. Higher rates of lichen sclerosus have been reported among twins and among family members.

The ICD-10 lists WSN under "other congenital malformations of mouth". It could be classified as a skin condition, or more precisely as a genodermatosis (a genetically determined skin disorder).

The cause of the condition is unknown. The disease is characterized by non-caseating granulomatous inflammation. That is, the granulomas do not undergo the caseating ("cheese-like") necrosis typical of the granulomas of tuberculosis.

There is disagreement as to whether OFG represents an early form of Crohn's disease or sarcoidosis, or whether it is a distinct, but similar clinical entity. Crohn's disease can affect any part of gastrointestinal tract, from mouth to anus. When it involves the mouth alone, some authors refer to this as "oral Crohn's disease", distinguishing it from OFG, and others suggest that OFG is the same condition as Crohn's disease when it presents in the oral cavity.

OFG may represent a delayed hypersensitivity reaction, but the causative antigen(s) is not identified or varies form one individual to the next. Suspected sources of antigens include metals, e.g. cobalt, or additives and preservatives in foods, including benzoates, benzoic acid, cinnamaldehyde, metabisulfates, butylated hydroxyanisole, dodecyl gallate, tartrazine, or menthol, Examples of foods which may contain these substances include margarine, cinnamon, eggs, chocolate or peppermint oil.

Some suggest that infection with atypical mycobacteria could be involved, (paratuberculosis), and that OFG is a reaction to mycobacterial stress protein mSP65 acting as an antigen.

In response to an antigen, a chronic, submucosal, T cell mediated inflammatory response occurs, which involves cytokines (e.g. tumor necrosis factor alpha), protease-activated receptors, matrix metalloproteinases and cyclooxygenases. The granulomas in OFG form in the lamina propria, and may form adjacent to or within lymphatic vessels. This is thought to cause obstruction of lymphatic drainage and lymphedema which is manifest as swelling clinically.

There may be a genetic predisposition to the condition. People who develop OFG often have a history of atopy, such as childhood asthma or eczema.

In developed countries, this disease occurs mostly in young adults. In developing countries, NUG may occur in children of low socioeconomic status, usually occurring with malnutrition (especially inadequate protein intake) and shortly after the onset of viral infections (e.g. measles).

Predisposing factors include smoking, viral respiratory infections and immune defects, such as in HIV/AIDS. Uncommon, except in lower socioeconomic classes, this typically affects adolescents and young adults, especially in institutions, armed forces, etc., or people with HIV/AIDS. The disease has occurred in epidemic-like patterns, but it is not contagious.

Although it is not clear what causes LS, several theories have been postulated. Lichen Sclerosus is not contagious; it cannot be caught from another person.

Several risk factors have been proposed, including autoimmune diseases, infections and genetic predisposition. There is evidence that LS can be associated with thyroid disease.

Dental plaque accumulates at the surfaces when proper cleaning and maintaining is not done. There is inflammation due to the bacteria released from the toxins. calculus forms and if not removed, causes this disease.

An examination by the dentist or dental hygienist should be sufficient to rule out the issues such as malnutrition and puberty. Additional corresponding diagnosis tests to certain potential disease may be required. This includes oral glucose tolerance test for diabetes mellitus, blood studies, human gonadotrophin levels for pregnancy, and X-rays for teeth and jaw bones.

In order to determine the periodontal health of a patient, the dentist or dental hygienist records the sulcular depths of the gingiva and observes any bleeding on probing. This is often accomplished with the use of a periodontal probe. Alternatively, dental floss may also be used to assess the Gingival bleeding index. It is used as an initial evaluation on patient's periodontal health especially to measure gingivitis. The number of bleeding sites is used to calculate the gingival bleeding score.

Peer-reviewed dental literature thoroughly establishes that bleeding on probing is a poor positive predictor of periodontal disease, but conversely lack of bleeding is a very strong negative predictor. The clinical interpretation of this research is that while BOP presence may not indicate periodontal disease, continued absence of BOP is a strong predictor (approximately 98%) of continued periodontal health.

Drug-related gingival hyperplasia is a cutaneous condition characterized by enlargement of the gums noted during the first year of drug treatment. There are three drug classes that are associated with this condition namely, anticonvulsants (such as phenyotoin and phenobartibal), calcium channel blocker (such as amlopidine, nifedipine and verapamil) and ciclosporin, an immunosuppressant Although the mechanism of drug related gingival hyperplasia is not well understood, some risk factors for the condition include the duration of drug use and poor oral hygiene. In most cases, alternative drugs are given, in order to avoid this side effect.

A wide variety of possible causes and treatments for vulvodynia are currently being explored. Moreover, there are probably several causes of vulvodynia, and some may be individual to the patient.

Possible causes include Sjogren's syndrome, the symptoms of which include chronic vaginal dryness. Others include genetic predisposition to inflammation, allergy or other sensitivity (for example: oxalates in the urine), an autoimmune disorder similar to lupus erythematosus or to eczema or to lichen sclerosus, infection (e.g., yeast infections, bacterial vaginosis, HPV, HSV), injury, and neuropathy—including an increased number of nerve endings in the vaginal area. Some cases seem to be negative outcomes of genital surgery, such as a Labioplasty. Initiation of hormonal contraceptives that contain low- dose estrogen before the age of 16 could predispose women to vulvar vestibulitis syndrome. A significantly lower pain threshold, especially in the posterior vestibulum, has also been associated with the use of hormonal contraceptives in women without vulvar vestibulitis syndrome. Pelvic floor dysfunction may be the underlying cause of some women's pain.

Chronic periapical periodontitis, also termed chronic apical periodontitis, chronic periradicular periodontitis, or assymptomatic periapical periodontitis

A periapical granuloma (also termed an apical granuloma or a radicular granuloma) is mass of chronically inflamed granulation tissue that forms at the apex of the root of a nonvital (dead) tooth. However, a periapical granuloma does not contain granulomatous inflammation, and therefore is not a true granuloma, but the term "periapical granuloma" is in common use.