There may or may not be any evidence of history of HGF in the family nor any usage of taking long-term medicines for any particular disease when it comes to diagnosing HGF. There also may or may not be any signs of medical and/or family history of mental retardation, hypertrichosis, nor clinical symptoms that can be associated with gingival enlargement. Although, enlargement of gingiva, interdental papilla, hindered speech, and secondary inflammatory changes taking place in the mouth commonly at the marginal gingiva are all very indicative of this condition. Commonly the patient will have mandiblular and maxilliary inflammation and overgrowth as opposed to the traditional pink, firm, and fleshy consistency of healthy gingiva. The patient's jaw may also appear distorted because of the gingiva englargements. Overgrowth of the gingiva can range from slightly covering the surface of teeth or it can even completely cover the surrounding teeth. The patient can also experience damage or loss of teeth.

Hereditary gingival fibromatosis (HGF), also known as idiopathic gingival hyperplasia, is a rare condition of gingival overgrowth. HGF is characterized as a benign, slowly progressive, nonhemorrhagic, fibrous enlargement of keratinized gingiva. It can cover teeth in various degrees, and can lead to aesthetic disfigurement. Fibrous enlargement is most common in areas of maxillary and mandibular tissues of both arches in the mouth. Phenotype and genotype frequency of HGF is 1:175,000 where males and females are equally affected but the cause is not entirely known. It mainly exists as an isolated abnormality but can also be associated with a multi-system syndrome.

It presents itself in the mouth, most frequently as a thick, bilateral, symmetrical white plaques with a spongy, corrugated or velvety texture. Most usually, the lesions are on the buccal mucosa, but sometimes on the labial mucosa, alveolar ridge, floor of the mouth, ventral surface of the tongue or soft palate. The gingival margin and dorsum of the tongue are almost never affected. Less commonly, sites outside the mouth are affected, including the nasal, esophageal, laryngeal, anal and genital mucosae. It usually is present from birth, or develops during childhood. Rarely, the lesions may develop during adolescence. Apart from the appearance of the affected areas, there are usually no other signs or symptoms.

White sponge nevus (WSN, or white sponge naevus, Cannon's disease, hereditary leukokeratosis of mucosa, white sponge nevus of Cannon, familial white folded dysplasia, or oral epithelial nevus), is an autosomal dominant condition of the oral mucosa (the mucous membrane lining of the mouth). It is caused by a mutations in certain genes coding for keratin, which causes a defect in the normal process of keratinization of the mucosa. This results in lesions which are thick, white and velvety on the inside of the cheeks within the mouth. Usually, these lesions are present from birth or develop during childhood. The condition is entirely harmless, and no treatment is required.

Clinically, three distinct patterns of palmoplantar keratoderma may be identified: diffuse, focal, and punctate.

Diffuse palmoplantar keratoderma is a type of palmoplantar keratoderma that is characterized by an even, thick, symmetric hyperkeratosis over the whole of the palm and sole, usually evident at birth or in the first few months of life. Restated, diffuse palmoplantar keratoderma is an autosomal dominant disorder in which hyperkeratosis is confined to the palms and soles. The two major types can have a similar clinical appearance:

- "Diffuse epidermolytic palmoplantar keratoderma" (also known as "Palmoplantar keratoderma cum degeneratione granulosa Vörner," "Vörner's epidermolytic palmoplantar keratoderma", and "Vörner keratoderma") is one of the most common patterns of palmoplantar keratoderma, an autosomal dominant condition that presents within the first few months of life, characterized by a well-demarcated, symmetric thickening of palms and soles, often with a "dirty" snakeskin appearance due to underlying epidermolysis.

- "Diffuse nonepidermolytic palmoplantar keratoderma" (also known as "Diffuse orthohyperkeratotic keratoderma," "Hereditary palmoplantar keratoderma," "Keratosis extremitatum progrediens," "Keratosis palmoplantaris diffusa circumscripta," "Tylosis," "Unna–Thost disease", and "Unna–Thost keratoderma") is inherited as an autosomal dominant condition and is present from infancy, characterized by a well-demarcated, symmetric, often "waxy" keratoderma involving the whole of the palms and soles.

Common symptoms include:

- Excess keratin in nail beds and thickening of the nails

- Hyperkeratosis on hands and feet

- Oral lesions that look like thick white plaques

- Steatocystoma multiplex

- Pain

- Blisters

AI can be classified according to their clinical appearances:

- Type 1 - Hypoplastic

Enamel of abnormal thickness due to malfunction in enamel matrix formation. Enamel is very thin but hard & translucent, and may have random pits & grooves. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel differs in appearance from dentine radiographically as normal functional enamel.

- Type 2 - Hypomaturation

Enamel has sound thickness, with a pitted appearance. It is less hard compared to normal enamel, and are prone to rapid wear, although not as intense as Type 3 AI. Condition is of autosomal dominant, autosomal recessive, or x-linked pattern. Enamel appears to be comparable to dentine in its radiodensity on radiograpshs.

- Type 3 - Hypocalcified

Enamel defect due to malfunction of enamel calcification, therefore enamel is of normal thickness but is extremely brittle, with an opaque/chalky presentation. Teeth are prone to staining and rapid wear, exposing dentine. Condition is of autosomal dominant and autosomal recessive pattern. Enamel appears less radioopaque compared to dentine on radiographs.

- Type 4: Hypomature hypoplastic enamel with taurodontism

Enamel has a variation in appearance, with mixed features from Type 1 and Type 2 AI. All Type 4 AI has taurodontism in common. Condition is of autosomal dominant pattern.

Other common features may include an anterior open bite, taurodontism, sensitivity of teeth.

Differential diagnosis would include dental fluorosis, molar-incisor hypomineralization, chronological disorders of tooth development.

Amelogenesis imperfecta (AI) is a congenital disorder that presents with a rare abnormal formation of the enamel or external layer of the crown of teeth, unrelated to any systemic or generalized conditions. Enamel is composed mostly of mineral, that is formed and regulated by the proteins in it. Amelogenesis imperfecta is due to the malfunction of the proteins in the enamel (ameloblastin, enamelin, tuftelin and amelogenin) as a result of abnormal enamel formation via amelogenesis.

People afflicted with amelogenesis imperfecta have teeth with abnormal color: yellow, brown or grey; this disorder can afflict any number of teeth of both dentitions. The teeth have a lower risk for dental cavities and are hypersensitive to temperature changes as well as rapid attrition, excessive calculus deposition, and gingival hyperplasia.

HIES often appears early in life with recurrent staphylococcal and candidal infections, pneumonias, and eczematoid skin.

- Autosomal dominant Hyper-IgE Syndrome caused by STAT3 defects, called Job Syndrome, have characteristic facial, dental, and skeletal abnormalities. Patients with STAT3 HIES may have either delay of or failure in shedding of primary teeth. The characteristic facial features are usually set by age 16. These include facial asymmetry, a prominent forehead, deep-set eyes, a broad nasal bridge, a wide, fleshy nasal tip, and mild prognathism. Additionally, facial skin is rough with prominent pores. Finally, some patients with STAT3 HIES have scoliosis, as well as bones that fracture easily.

- Autosomal recessive

It is characterized by recurrent "cold" staphylococcal infections, unusual eczema-like skin rashes, severe lung infections that result in pneumatoceles (balloon-like lesions that may be filled with air or pus or scar tissue) and very high concentrations of the serum antibody IgE. Inheritance can be autosomal dominant or autosomal recessive. Many patients with autosomal dominant STAT3 hyper-IgE syndrome have characteristic facial and dental abnormalities, fail to lose their primary teeth, and have two sets of teeth simultaneously.

Worth syndrome, also known as benign form of Worth hyperostosis corticalis generalisata with torus platinus, autosomal dominant osteosclerosis, autosomal dominant endosteal hyperostosis or Worth disease, is a rare autosomal dominant congenital disorder that is caused by a mutation in the LRP5 gene. It is characterized by increased bone density and benign bony structures on the palate.

Gingival enlargement, (also termed gingival overgrowth, hypertrophic gingivitis, gingival hyperplasia, or gingival hypertrophy, and sometimes abbreviated to GO), is an increase in the size of the gingiva (gums). It is a common feature of gingival disease. Gingival enlargement can be caused by a number of factors, including inflammatory conditions and the side effects of certain medications. The treatment is based on the cause. A closely related term is epulis, denoting a localized tumor (i.e. lump) on the gingiva.

The terms gingival hyperplasia and gingival hypertrophy have been used to describe this topic in the past. These are not precise descriptions of gingival enlargement because these terms are strictly histologic diagnoses, and such diagnoses require microscopic analysis of a tissue sample. Hyperplasia refers to an increased number of cells, and hypertrophy refers to an increase in the size of individual cells. As these identifications obviously cannot be performed with a clinical examination and evaluation of the tissue, the term "gingival enlargement" is more properly applied. Gingival enlargement has been classified according to cause into 5 general groups:

- Inflammatory enlargement

- Drug induced enlargement

- Enlargement associated with systemic diseases or conditions

- Neoplastic enlargement

- False enlargement.

Focal palmoplantar and gingival keratosis is a rare autosomal dominant disease whose clinical features, and in particular, pathologic alterations and molecular mechanisms remains to be well defined.

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 symptoms of ichthyosis hystrix Curth-Macklin are similar to epidermolytic hyperkeratosis (NPS-2 type) but there is no blistering and the hyperkeratosis is verrucous or spine-like. The hyperkeratosis is brown-grey in colour and is most obvious on the arms and legs. It is an autosomal dominant condition and can be caused by errors to the KRT1 gene. It is named after Helen Ollendorff Curth (1899-1982), a German-Jewish dermatologist, and Madge Thurlow Macklin (1893–1962), an American medical geneticist, and is one of the first syndromes named after two women.

Ichthyosis hystrix is a group of rare skin disorders in the ichthyosis family of skin disorders characterized by massive hyperkeratosis with an appearance like spiny scales. This term is also used to refer to a type of epidermal nevi with extensive bilateral distribution.

This type of epulis is neither pyogenic ("pus producing") nor a true granuloma, but it is a vascular lesion. About 75% of all pyogenic granulomas occur on the gingiva, although they may also occur elsewhere in the mouth or other parts of the body (where the term epulis is inappropriate). This common oral lesion is thought to be a reaction to irritation of the tissues and poor oral hygiene. It is more common in younger people and in females, and appears as a red-purple swelling and bleeds easily.

Gingival cyst of adult is a rare condition. The incidence is less than 0.5%. It is formed from the rests of dental lamina. It is found in the soft tissues on the buccal and labial portions of the jaw. It usually occurs on the facial gingiva as a single small flesh colored swelling, sometimes with a bluish hue due to the cystic fluid. Sometimes, it may occur in cluster, either unilaterally or bilaterally or on the lingual surface of the alveolar process. It is most commonly seen in the canine and premolar regions of the mandible, and are sometimes confused with lateral periodontal cysts. It is not normally problematic, but when it grows larger, it can cause some discomfort. It can be removed by simple surgical excision. They are developed late in life, generally up to the sixth decade of age.

Juvenile hyaline fibromatosis (also known as "Fibromatosis hyalinica multiplex juvenilis," "Murray–Puretic–Drescher syndrome") is a very rare, autosomal recessive disease due to mutations in capillary morphogenesis protein-2 (CMG-2 gene). It occurs from early childhood to adulthood, and presents as slow-growing, pearly white or skin-colored dermal or subcutaneous papules or nodules on the face, scalp, and back, which may be confused clinically with neurofibromatosis.

Epulis (; plural "epulides") is any tumor like enlargement (i.e. lump) situated on the gingival or alveolar mucosa. The word literally means "(growth) on the gingiva", and describes only the location of the mass and has no further implications on the nature of the lesion. There are three types: fibromatous, ossifying and acanthomatous. The related term parulis (commonly called a gumboil) refers to a mass of inflamed granulation tissue at the opening of a draining sinus on the alveolus over (or near to) the root of an infected tooth. Another closely related term is gingival enlargement, which tends to be used where the enlargement is more generalized over the whole gingiva rather than a localized mass.

Plantar fibromatosis is most frequently present on the medial border of the sole, near the highest point of the arch. The lump is usually painless and the only pain experienced is when the nodule rubs on the shoe or floor. The overlying skin is freely movable, and contracture of the toes does not occur in the initial stages.

The typical appearance of plantar fibromatosis on magnetic resonance imaging (MRI) is a poorly defined, infiltrative mass in the aponeurosis next to the plantar muscles.

Only 25% of patients show symptoms on both feet (bilateral involvement). The disease may also infiltrate the dermis or, very rarely, the flexor tendon sheath

Gum recession is generally not an acute condition. In most cases, receding of gums is a progressive condition that occurs gradually over the years. This is one reason that it is common over the age of 40. Because the changes in the condition of the gums from one day to another are minimal, patients get used to the gums' appearance and tend not to notice the recession visually. Receding gums may remain unnoticed until the condition starts to cause symptoms.

The following signs and symptoms may indicate gum recession:

- Tooth mobility

- Dentin hypersensitivity (over-sensitive teeth) - short, sharp pain is triggered by hot, cold, sweet, sour, or spicy food and drink. If the cementum covering the root is not protected anymore by the gums, it is easily abraded exposing the dentin tubules to external stimuli.

- Teeth may also appear longer than normal (a larger part of the crown is visible if gums are receding)

- The roots of the tooth are exposed and visible

- The tooth feels notched at the gum line

- Change in the tooth’s color (due to the color difference between enamel and cementum)

- Spaces between teeth seem to grow (the space is the same, but it seems larger because the gums do not fill it any more)

- Cavities below the gum line

If the gum recession is caused by gingivitis, the following symptoms may also be present:

- Puffy, red, or swollen (inflamed) gums

- Gum bleeding while brushing or flossing

- Bad breath (halitosis)

In some cases, it is the treatment of gingivitis that reveals a gum recession problem, that was previously masked by the gums swelling.

Pachyonychia congenita may be divided into these types:

- Pachyonychia congenita type I (also known as "Jadassohn–Lewandowsky syndrome") is an autosomal dominant keratoderma that principally involves the plantar surfaces, but also with nails changes that may be evident at birth, but more commonly develop within the first few months of life.

- Pachyonychia congenita type II (also known as "Jackson–Lawler pachyonychia congenita" and "Jackson–Sertoli syndrome") is an autosomal dominant keratoderma presenting with a limited focal plantar keratoderma that may be very minor, with nails changes that may be evident at birth, but more commonly develop within the first few months of life.