Plasma cell gingivits is rare, and plasma cell cheilitis is very rare. Most people with plasma cell cheilitis have been elderly.

Histologically plasma cell gingivitis shows mainly plasma cells. The differential diagnosis is with acute leukemia and multiple myeloma. Hence, blood tests are often involved in ruling out other conditions. A biopsy is usually taken, and allergy testing may also be used. The histopathologic appearance is characterized by diffuse, sub-epithelial plasma cell inflammatory infiltration into the connective tissue. The epithelium shows spongiosis. Some consider that plasmoacanthoma (solitary plasma cell tumor) is part of the same spectrum of disease as plasma cell cheilitis.

Chronic ulcerative stomatitis is a recently discovered condition with specific immunopathologic features. It is characterized by erosions and ulcerations which relapse and remit. Lesions are located on the buccal mucosa (inside of the cheeks) or on the gingiva (gums). The condition resembles Oral lichen planus when biopsied.

The diagnosis is made with Immunofluorescence techniques, which shows circulating and tissue-bound autoantibodies (particulate stratified squamous-epithelium-specific antinuclear antibody) to DeltaNp63alpha protein, a normal component of the epithelium. Treatment is with hydroxychloroquine.

Angular chielitis is normally a diagnosis made clinically. If the sore is unilateral, rather than bilateral, this suggests a local factor ("e.g.", trauma) or a split syphilitic papule. Angular cheilitis caused by mandibular overclosure, drooling, and other irritants is usually bilateral.

The lesions are normally swabbed to detect if Candida or pathogenic bacterial species may be present. Persons with angular cheilitis who wear dentures often also will have their denture swabbed in addition. A complete blood count (full blood count) may be indicated, including assessment of the levels of iron, ferritin, vitamin B12 (and possibly other B vitamins), and folate.

Angular cheilitis could be considered to be a type of cheilitis or stomatitis. Where Candida species are involved, angular cheilitis is classed as a type of oral candidiasis, specifically a primary (group I) Candida-associated lesion. This form angular cheilitis which is caused by Candida is sometimes termed "Candida-associated angular cheilitis", or less commonly, "monilial perlèche". Angular cheilitis can also be classified as acute (sudden, short-lived appearance of the condition) or chronic (lasts a long time or keeps returning), or refractory (the condition persists despite attempts to treat it).

Good oral hygiene (thorough tooth brushing and flossing and regular professional cleaning and examination) may be helpful to prevent these disorders. Drinking plenty of water and the production of enough saliva, aid in the reduction of bacterial growth. Minimizing irritants or injury in the mouth when possible can aid in the prevention of glossitis. Avoiding excessive use of any food or substance that irritates the mouth or tongue may also help.

The diagnosis can typically be made from the clinical appearance alone, but not always. As candidiasis can be variable in appearance, and present with white, red or combined white and red lesions, the differential diagnosis can be extensive. In pseudomembraneous candidiasis, the membranous slough can be wiped away to reveal an erythematous surface underneath. This is helpful in distinguishing pseudomembraneous candidiasis from other white lesions in the mouth that cannot be wiped away, such as lichen planus, oral hairy leukoplakia. Erythematous candidiasis can mimic geographic tongue. Erythematous candidiasis usually has a diffuse border that helps distinguish it from erythroplakia, which normally has a sharply defined border.

Special investigations to detect the presence of candida species include oral swabs, oral rinse or oral smears. Smears are collected by gentle scraping of the lesion with a spatula or tongue blade and the resulting debris directly applied to a glass slide. Oral swabs are taken if culture is required. Some recommend that swabs be taken from 3 different oral sites. Oral rinse involves rinsing the mouth with phosphate-buffered saline for 1 minute and then spitting the solution into a vessel that examined in a pathology laboratory. Oral rinse technique can distinguish between commensal candidal carriage and candidiasis. If candidal leukoplakia is suspected, a biopsy may be indicated. Smears and biopsies are usually stained with periodic acid-Schiff, which stains carbohydrates in fungal cell walls in magenta. Gram staining is also used as Candida stains are strongly Gram positive.

Sometimes an underlying medical condition is sought, and this may include blood tests for full blood count and hematinics.

If a biopsy is taken, the histopathologic appearance can be variable depending upon the clinical type of candidiasis. Pseudomembranous candidiasis shows hyperplastic epithelium with a superficial parakeratotic desquamating (i.e., separating) layer. Hyphae penetrate to the depth of the stratum spinosum, and appear as weakly basophilic structures. Polymorphonuclear cells also infiltrate the epithelium, and chronic inflammatory cells infiltrate the lamina propria.

Atrophic candidiasis appears as thin, atrophic epithelium, which is non-keratinized. Hyphae are sparse, and inflammatory cell infiltration of the epithelium and the lamina propria. In essence, atrophic candidiasis appears like pseudomembranous candidiasis without the superficial desquamating layer.

Hyperplastic candidiasis is variable. Usually there is hyperplastic and acanthotic epithelium with parakeratosis. There is an inflammatory cell infiltrate and hyphae are visible. Unlike other forms of candidiasis, hyperplastic candidiasis may show dysplasia.

The diagnosis is usually made by tissue biopsy, however this cannot reliably distinguish between the granulomas of OFG and those of Crohn's disease or sarcoidosis. Other causes of granulomatous inflammation are ruled out, such as sarcoidosis,

Crohn's disease, allergic or foreign body reactions and mycobacterial infections.

Terms such as "plasma cell gingivostomatitis", "atypical gingivostomatitis" and "idiopathic gingivostomatitis" are sometimes a synonym for plasma cell gingivitis, or specifically to refer to a severe form of plasma cell gingivitis.

Anti-tumour necrosis factor α antagonists (e.g. infliximab)

Dietary restriction of a particular suspected or proven antigen may be involved in the management of OFG, such as cinnamon or benzoate-free diets.

Strawberry tongue (also called raspberry tongue), refers to glossitis which manifests with hyperplastic (enlarged) fungiform papillae, giving the appearance of a strawberry. White strawberry tongue is where there is a white coating on the tongue through which the hyperplastic fungiform papillae protrude. Red strawberry tongue is where the white coating is lost and a dark red, erythematous surface is revealed, interspaced with the hyperplastic fungiform papillae. White strawberry tongue is seen in early scarlet fever (a systemic infection of group A β- hemolytic streptococci), and red strawberry tongue occurs later, after 4–5 days. Strawberry tongue is also seen in Kawasaki disease (a vasculitic disorder primarily occurring in children under 5), and toxic shock syndrome. It may mimic other types of glossitis or Vitamin B12 deficiency.

This is a rare inflammatory condition of the minor salivary glands, usually in the lower lip, which appears swollen and everted. There may also be ulceration, crusting, abscesses, and sinus tracts. It is an acquired disorder, but the cause is uncertain. Suspected causes include sunlight, tobacco, syphilis, poor oral hygiene and genetic factors. The openings of the minor salivary gland ducts become inflamed and dilated, and there may be mucopurulent discharge from the ducts. A previous classification suggested dividing cheilitis into 3 types based on severity, with the later stages involving secondary infection with bacteria, and increased ulceration, suppuration and swelling: Type 1, Simple; Type 2, Superficial suppurative ("Baelz's disease"); and Type 3, Deep suppurative ("cheilitis glandularis epostemetosa"). Cheilitis glandularis usually occurs in middle-aged and elderly males, and it carries a risk of malignant transformation to squamous cell carcinoma (18% to 35%). Preventative treatment such as vermilionectomy ("lip shave") is therefore the treatment of choice.

The severity of oral candidiasis is subject to great variability from one person to another and in the same person from one occasion to the next. The prognosis of such infection is usually excellent after the application of topical or systemic treatments. However, oral candidiasis can be recurrent. Individuals continue to be at risk of the condition if underlying factors such as reduced salivary flow rate or immunosuppression are not rectifiable.

Candidiasis can be a marker for underlying disease, so the overall prognosis may also be dependent upon this. For example, a transient erythematous candidiasis that developed after antiobiotic therapy usually resolves after antibiotics are stopped (but not always immediately), and therefore carries an excellent prognosis—but candidiasis may occasionally be a herald of a more sinister undiagnosed pathology, such as HIV/AIDS or leukemia.

It is possible for candidiasis to spread to/from the mouth, from sites such as the pharynx, esophagus, lungs, liver, anogenital region, skin or the nails. The spread of oral candidiasis to other sites usually occurs in debilitated individuals. It is also possible that candidiasis is spread by sexual contact. Rarely, a superficial candidal infection such as oral candidiasis can cause invasive candidiasis, and even prove fatal. The observation that Candida species are normally harmless commensals on the one hand, but are also occasionally capable of causing fatal invasive candidiases has led to the description "Dr Jekyll and Mr Hyde".

The role of thrush in the hospital and ventilated patients is not entirely clear however there is a theoretical risk of positive interaction of candida with topical bacteria that could increase the risk for Ventilator Associated Pneumonia and other diseases.

Also termed "lip dermatitis", eczematous cheilitis is a diverse group of disorders which often have an unknown cause. Chronic eczematous reactions account for the majority of chronic cheilitis cases.

It is divided into endogenous (due to an inherent characteristic of the individual), and exogenous (where it is caused by an external agent). The main cause of endogenous eczematous cheilitis is atopic cheilitis (atopic dermatitis), and the main causes of exogenous eczematous cheilitis is irritant contact cheilitis ("e.g.", caused by a lip-licking habit) and allergic contact cheilitis. The latter is characterized by a dryness, fissuring, edema, and crusting. It affects females more commonly than males, in a ratio of about 9:1.

The most common causes of allergic contact cheilitis is lip cosmetics, including lipsticks and lip balm, followed by toothpastes. A lipstick allergy can be difficult to diagnose in some cases as it is possible that cheilitis can develop without the person even wearing lipstick. Instead, small exposure such as kissing someone who is wearing lipstick is enough to cause the condition.

Allergy to Balsam of Peru can manifest as cheilitis. Allergies to metal, wood, or other components can cause cheilitis reactions in musicians, especially players of woodwind and brass instruments, "e.g.", the so-called "clarinetist's cheilitis", or "flutist's cheilitis". "Pigmented contact cheilitis" is one type of allergic cheilitis in which a brown-black discoloration of the lips develops. Patch testing is used to identify the substance triggering allergic contact cheilitis.

This condition is considered premalignant because it may lead to squamous cell carcinoma in about 10% of all cases. It is not possible to predict which cases will progress into SCC, so the current consensus is that all lesions should be treated.

Treatment options include 5-fluorouracil, imiquimod, scalpel vermillionectomy, chemical peel, electrosurgery, and carbon dioxide laser vaporization. These curative treatments attempt to destroy or remove the damaged epithelium. All methods are associated with some degree of pain, edema, and a relatively low rate of recurrence.

To prevent AC from developing, protective measures could be undertaken such as avoiding mid-day sun, or use of a broad-brimmed hat, lip balm with anti UVA and UVB ingredients (e.g. para-aminobenzoic acid), or sun blocking agents (e.g. zinc oxide, titanium oxide) prior to sun exposure.

BMS is a diagnosis of exclusion, i.e. all other explanations for the symptoms are ruled out before the diagnosis is made. There are no clinically useful investigations that would help to support a diagnosis of BMS (by definition all tests would have normal results), but blood tests and / or urinalysis may be useful to rule out anemia, deficiency states, hypothyroidism and diabetes. Investigation of a dry mouth symptom may involve sialometry, which objectively determines if there is any reduction of the salivary flow rate (hyposalivation). Oral candidiasis can be tested for with use of a swabs, smears, an oral rinse or saliva samples. It has been suggested that allergy testing ("e.g.", patch test) is inappropriate in the absence of a clear history and clinical signs in people with a burning sensation in the mouth. The diagnosis of a people with a burning symptom may also involve psychologic screening e.g. depression questionnaires.

The second edition of the International Classification of Headache Disorders lists diagnostic criteria for "Glossodynia and Sore Mouth":

BMS is benign (importantly, it is not a symptom of oral cancer), but as a cause of chronic pain which is poorly controlled, it can detriment quality of life, and may become a fixation which cannot be ignored, thus interfering with work and other daily activities. Two thirds of people with BMS have a spontaneous partial recovery six to seven years after the initial onset, but in others the condition is permanent. Recovery is often preceded by a change in the character of the symptom from constant to intermittent. No clinical factors predicting recovery have been noted.

If there is an identifiable cause for the burning sensation (i.e. primary BMS), then psychologic dysfunctions such as anxiety and depression often disappear if the symptom is successfully treated.

Immunohistochemistry is unnecessary for the diagnosis, but will highlight a mixed B- and T-cell population within the lymphoid component, without light chain (kappa or lambda) restriction. Any muscle markers would be negative.

The lesion presents in young patients, so the differential for a "polyp", especially when the lymphoid component is crushed or dominant, would include a rhabdomyosarcoma, extramedullary plasmacytoma, and a neuroendocrine adenoma of the middle ear.

In terms of diagnosis of "humoral immune deficiency" depends upon the following:

- Measure "serum immunoglobulin levels"

- B cell count

- Family medical history

Several other illnesses can present with a monoclonal gammopathy, and the monoclonal protein may be the first discovery before a formal diagnosis is made:

The majority (90%) of cases have not had detectable cytogenetic abnormalities. Most importantly, the Philadelphia chromosome and other BCR/ABL fusion genes are not detected.

Treatment for "B cell deficiency"(humoral immune deficiency) depends on the cause, however generally the following applies:

- Treatment of infection(antibiotics)

- Surveillance for malignancies

- Immunoglobulin replacement therapy

Hepatic infiltrates can be found in either the sinusoids, portal triad regions, or both.