Treatment for TRs is limited to tooth extraction because the lesion is progressive. Amputation of the tooth crown without root removal has also been advocated in cases demonstrated on a radiograph to be type 2 resorption without associated periodontal or endodontic disease because the roots are being replaced by bone. However, X-rays are recommended prior to this treatment to document root resorption and lack of the periodontal ligament.

Tooth restoration is not recommended because resorption of the tooth will continue underneath the restoration. Use of alendronate has been studied to prevent TRs and decrease progression of existing lesions.

There are two types of TR. "Type 1" lesions are focal defects often caused by local inflammation. "Type 2" lesions are characterized by a generalized loss of root radiopacity on a dental radiograph. The definitive cause of type 2 TRs is unknown, but histologically destruction of the cementum and other mineralized tissue of the tooth root by odontoclasts is seen. It occurs secondary to the loss of the protective covering of the root (the periodontal ligaments) and possibly to a stimulus such as periodontal disease and the release of cytokines, leading to odontoclast migration. However, FORLs can develop in the absence of inflammation. The natural inhibition to root resorption provided by the lining of the root may be altered by increased amounts of Vitamin D, in cats supplied by their diet.

The diagnosis is made clinically, and usually this is clear cut if the lesion is associated with the flange of a denture. Tissue biopsy is not usually indicated before removal of the lesion, since the excises surgical specimen is usually sent for histopathologic examination and the diagnosis is confirmed retrospectively. Rarely, incisional biopsy may be indicated to rule out neoplasia, e.g. in the presence of suspicious ulceration. The appearance may also be confused with pyogenic granuloma.

The excessive tissue is composed of cellular, inflamed fibrous connective tissue. The appearance of an epulis fissuratum microscopically is an overgrowth of cells from the fibrous connective tissue. The epithelial cells are usually hyperkeratotic and irregular, hyperplastic rete ridges are often seen.

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

The diagnosis is usually made on the clinical appearance, and tissue biopsy is not usually needed. The histologic picture is one of superficial candidal hyphal infiltration and a polymorphonuclear leukocytic inflammatory infiltrate present in the epithelium. The rete ridges are elongated and hyperplastic (pseudoepitheliomatous hyperplasia, which may be mistaken for carcinoma).

Diagnosis is mainly clinical, based on the history and clinical appearance. The differential diagnosis includes other oral white lesions such as Leukoplakia, squamous cell carcinoma, oral candidiasis, lichen planus, white sponge nevus and contact stomatitis. In contrast to pseudomembraneous candidiasis, this white patch cannot be wiped off. Tissue biopsy is sometimes carried out to rule out other lesions, although biopsy is not routinely carried out for this condition.

Differentiation between this and SCC would be based on a history of recent trauma or dental treatment in the area.

Immunohistochemistry may aid the diagnosis. If the lesion is NS, there will be focal to absent immunoreactivity for p53, low immunoreactivity for MIB1 (Ki-67), and the presence of 4A4/p63- and calponin-positive myoepithelial cells.

Tissue biopsy is usually indicated to rule out other causes of white patches and also to enable a detailed histologic examination to grade the presence of any epithelial dysplasia. This is an indicator of malignant potential and usually determines the management and recall interval. The sites of a leukoplakia lesion that are preferentially biopsied are the areas that show induration (hardening) and erythroplasia (redness), and erosive or ulcerated areas. These areas are more likely to show any dysplasia than homogenous white areas.

Brush biopsy/exfoliative cytology is an alternative to incisional biopsy, where a stiff brush is scraped against the lining of the mouth to remove a sample of cells. This is then made into a smear which can be examined microscopically. Sometimes the biopsy site can be selected with adjunct methods which aim to highlight areas of dysplasia. Toluidine blue staining, where the dye is preferentially retained by dysplastic tissue, is sometimes used, but there is high false positive rate. Other methods involve the use of illuminescence, relying on either the property of normal autoflorescent molecules in mucosa such as collagen and keratin which is lost from areas of dysplasia or carcinoma under blue light, or by initially staining of the mucosa with toluidine blue or dilute acetic acid and examination under white light.

Usually this lesion is reversible if the tobacco habit is stopped completely, even after many years of use. In one report, 98% of lesions disappeared within 2 weeks of stopping tobacco use. The risk of the lesion developing into oral cancer (generally squamous cell carcinoma and its variant verrucous carcinoma) is relatively low. Indeed, veruccous carcinoma is sometimes term snuff dipper's cancer. In most reported cases, malignant transformation has occurring in individuals with a very long history of chewing tobacco or who use dry snuff.

Smokeless tobacco use is also accompanied by increased risk of other oral conditions such as dental caries (tooth decay), periodontitis (gum disease), attrition (tooth wear) and staining.

Treatment may involve smoking cessation and prescription of topical or systemic antifungal medication. Usually the mucosal changes resolve with antifungal therapy, but sometimes the lesion is resistant to complete resolution.

The histologic appearance is similar to mucoceles from other locations. The spilled mucin causes a granulation tissue to form, which usually contains foamy histiocytes. Ultrasound and magnetic resonance imaging may be useful to image the lesion. A small squamous cell carcinoma obstructing the Wharton duct may require clinical examination to be distinguished from a ranula.

The lesion is usually present in children. Ranulas are the most common pathologic lesion associated with the sublingual glands.

Healing is prolonged, and usually takes 6–10 weeks. The ulcer heals by secondary intention.

Leukoplakia has a wide range of possible histologic appearances. The degree of hyperkeratosis, epithelial thickness (acanthosis/), dysplasia and inflammatory cell infiltration in the underlying lamina propria are variable. In mucous membranes, hyperkeratosis can be defined as "an increase in the thickness of the keratin layer of the epithelium, or the presence of such a layer in a site where none would normally be expected." In leukoplakia, the hyperkeratosis varies in thickness, and may be either ortho- or para-keratosis, (depending upon whether cell nuclei are lost or retained in the superficial layers respectively), or a mixture of both in different areas of the lesion.

The epithelium may show hypertrophy (e.g. acanthosis) or atrophy. Red areas within leukoplakia represent atrophic or immature epithelium which has lost the ability to keratinize. The transition between the lesion and normal surrounding mucosa may be well demarcated, or poorly defined. Melanin, a pigment naturally produced in oral mucosa, can leak from cells and give a grey color to some leukoplakia lesions.

Hyperkeratosis and altered epithelial thickness may be the only histologic features of a leukoplakia lesion, but some show dysplasia. The word "dysplasia" generally means "abnormal growth", and specifically in the context of oral red or white lesions refers to microscopic changes ("cellular atypia") in the mucosa that indicate a risk of malignant transformation. When dysplasia is present, there is generally an inflammatory cell infiltration in the lamina propria. The following are commonly cited as being possible features of epithelial dysplasia in leukoplakia specimens:

- Cellular pleomorphism, in which cells are of abnormal and different shapes.

- Nuclear atypia, in which the nuclei of cells varies in size, any may be increased in size relative to the cytoplasm, shape, and may stain more intensely. There may also be more prominent nucleoli.

- Increased number of cells seen undergoing mitosis, including both normal and abnormal mitoses. Abnormal mitosis may be abnormally located, e.g. occurring in suprabasal cells (cell layers more superficial to the basal cell layer) or of abnormal form, e.g. "tri-radiate mitoses" (a cell splitting into 3 daughter cells rather than only 2)

- Loss the normal organization of the epithelial layers. The distinction between the epithelial layers may be lost. Normally stratified squamous epithelium shows progressive changes in the form of cells from the basal to the superficial layers, with cells becoming more flat ("squames") towards the surface as a continuous maturation process. In dysplastic epithelium, cells may become vertically orientated rather than becoming flat towards the surface.

- There may be abnormal keratinization, where keratin is formed below the normal keratin layer. This can occur in individual cells or groups of cells, forming an intraepithelial keratin pearl. There may be an increase in number of basal cells, and they may lose their cellular orientation (losing their polarity and long axis).

- Alteration of the normal epithelial-connective tissue architecture - the rete pegs may become "drop shaped". wider at their base than more superficially.

Generally dysplasia is subjectively graded by pathologists into mild, moderate or severe dysplasia. This requires experience as it is a difficult skill to learn. It has been shown that there is high degree of inter-observer variation and poor reproducibility in how dysplasia is graded. Severe dysplasia is synonymous with the term carcinoma in situ, denoting the presence of neoplastic cells which have not yet penetrated the basement membrane and invaded other tissues.

An epulis granulomatosa is a granuloma which grows from an extraction socket (the hole left after a tooth has been removed), and as such can be considered to be a complication of healing after oral surgery.

Placing the cat's water in a shallow dish may prevent the chin from absorbing the bacteria in the water while the cat is drinking. If the cat is allergic to plastics or dyes, using a stainless-steel or glass dish is recommended . Cats may also have food allergies that make the development of acne more likely, so that switching kibble, or changing to a hydrolysed diet may be effective. Maintaining good hygiene and grooming habits make the development of feline acne less likely. Washing and exfoliating the chin with a gentle benzoyl-peroxide solution also may be preventive of further outbreaks.

The white lesion cannot be wiped away, unlike some other common oral white lesions, e.g. pseudomembranous candidiasis, and this may aid in the diagnosis. Diagnosis of OHL is mainly clinical, but can be supported by proof of EBV in the lesion (achieved by in situ hybridization, polymerase chain reaction, immunohistochemistry, Southern blotting, or electron microscopy) and HIV serotesting. When clinical appearance alone is used to diagnose OHL, there is a false positive rate of 17% compared to more objective methods. The appearance of OHL in a person who is known to be infected with HIV does not usually require further diagnostic tests as the association is well known. OHL in persons with no known cause of immunocompromise usually triggers investigations to look for an underlying cause. If tissue biopsy is carried out, the histopathologic appearance is of hyperlastic and parakeratinized epithelium, with "balloon cells" (lightly staining cells) in the upper stratum spinosum and "nuclear beading" in the superficial layers (scattered cells with peripheral margination of chromatin and clear nuclei, created by displacement of chromatin to the peripheral nucleus by EBV replication). Candida usually is seen growing in the parakeratin layer, but there are no normal inflammatory reactions to this in the tissues. There is no dysplasia (OHL is not a premalignant lesion).

This rare epulis (also called granular cell tumor or congenital gingival granular cell tumor) is not acquired, which is in contrast to most other epulides which tend to be reactive lesions to tissue irritation. It is also called Neumann's tumor. It has an unusual resemblance to granular cell myoblastoma. It is more common in the maxilla than the mandible. It is usually a pedunculated lesion in the incisor region.

Topical treatments such as warm compresses to the chin area may be sufficient for mild cases. Veterinary intervention may be required for treatment if secondary infection occurs. In this case, treatment may begin with clinical drainage of the pustules and a course of oral antibiotics.

Clearing the acne can be accomplished using an old toothbrush or flea comb (one designated for this purpose) and brush the cat's chin. This will loosen debris and remove dried scabs. Cleansing pads containing salicylic acid can be rubbed gently and allowed to air dry on the affected area. This may dissolve the oil that is clogging skin pores. Epsom-salt compresses applied twice daily dry the affected area to relieve the inflammation and itchiness.

There are many other conditions that are similar in appearance and must be ruled out before a diagnosis of erythroplakia is made (see table). Sometimes, a diagnosis is delayed for up to two weeks in order to see if the lesion spontaneously regresses on its own or if another cause can be found. Erythroplakia frequently is associated with dysplasia, and is thus a precancerous lesion.

The oral lesion itself is benign and self-limiting, however this may not necessarily be the case for the underlying cause of immunocompromise. For instance, OHL with HIV/AIDS is a predictor of bad prognosis, (i.e. severe immunosuppression and advanced disease).

Treatment involves biopsy of the lesion to identify extent of dysplasia. Complete excision of the lesion is sometimes advised depending on the histopathology found in the biopsy. Even in these cases, recurrence of the erythroplakia is common and, thus, long-term monitoring is needed.

Giant osteoclasts can occur in some diseases, including Paget's disease of bone and bisphosphonate toxicity.

The basis of management is to find and correct the underlying cause. Many times cats with EGC will respond to treatment with corticosteroids or to ciclosporin.

The cat must have a supply of niacin, as cats cannot convert tryptophan into niacin like dogs. However, diets high in corn and low in protein can result in skin lesions and scaly, dry, greasy skin, with hair loss. Another B vitamin, biotin, if deficient causes hair loss around the eyes and face. A lack of B vitamins can be corrected by supplementing with a vitamin B complex, and brewers yeast.