• Nondescript nodule with a history of trauma; common on lip; related to injection of dermal fillers

• Proliferation of epithelioid histiocytes and foreign body giant cells, nonnecrotizing; refractile or nonrefractile foreign material may be identified (Fig. 8-1).

• Poly-l-lactic acid fillers are refractile fusiform or geometric structures (Fig. 8-2).

• Lipid and silicone granulomas have cytoplasmic vacuoles of varying sizes (Figs. 8-3 and 8-4).

• Calcium hydroxylapatite consists of gray-brown microspheres, 25 to 40 microns in diameter, that are nonrefractile; they stimulate endogenous collagen production and are resorbed within a few months, but they may cause a granulomatous response (Fig. 8-5).

• Foreign body granulomas are common in odontogenic cysts (see Chapter 14), around amalgam tattoos (see Chapter 9), and in keratinizing squamous cell carcinomas (see Chapter 11).

• Hyaluronic acid fillers appear as amorphous basophilic pools of ground substance that stains for alcian blue and colloidal iron; they do not incite a reaction (Fig. 8-6).

• Palisaded granulomas of necrobiosis lipoidica, granuloma annulare, and rheumatoid arthritis are rarely encountered intraorally.

• Lipid granulomas may resemble atypical lipomatous tumors.

• Excision is curative.

• Generally affects young adults; lips show diffuse or localized rubbery swelling that does not remit (unlike angioedema); tissues feel tight and sore (Fig. 8-7, A and B).

• May also show concomitant swelling of the gingiva; long-standing cases show cobblestoning and fissuring of mucosa from edema.

• Melkersson-Rosenthal syndrome, in addition to the lip swelling, exhibits fissured tongue and facial palsy; because fissured tongue is very common and facial palsy in this syndrome is very rare, it is unclear if this is a true syndrome.

• Crohn disease—in addition to the aforementioned features, there may also be papular folds of tissue in the maxillary and mandibular sulci, aphthous-like ulcers, gastrointestinal symptoms, and thickened and erythematous appearance of perivermilion skin (see Fig. 8-7, C); oral findings precede the diagnosis of intestinal disease in 50% of cases; some patients may also present with pyostomatitis vegetans (see later).

• Nonnecrotizing granulomas are noted and may be subtle in early disease (especially in idiopathic orofacial granulomatosis) (Fig. 8-8) or more florid in later disease; granulomas of Crohn disease may occur in salivary glands and may contain eosinophils (Figs. 8-9 and 8-10); multiple levels should be performed, if necessary, through the entire block to locate granulomas; edema and chronic inflammation alone are not sufficient for the diagnosis.

• Other granulomatous processes must be ruled out with histochemical stains.

• Granulomas of sarcoidosis are nonnecrotizing and well demarcated or “naked” (Fig. 8-11); patients are often blacks, have hilar lymphadenopathy, and elevated levels of angiotensin-converting enzyme; labial salivary gland biopsies show granulomas in 33% of cases.

• Patch test for the idiopathic type to determine if hypersensitivity to the environment exists; intralesional steroid injections can be done every week for several weeks, but relapse is common; topical, intralesional, and systemic therapy controls disease in 70% of patients; minocycline or thalidomide helps some patients.

• Gastrointestinal work-up is indicated if there are intestinal symptoms.

• Shallow ulcers and erosions, miliary abscesses and pustules on erythematous mucosa (Fig. 8-12); vegetations may be a feature; sometimes folding and fissuring of the buccal mucosa occurs.

• Most common associations are ulcerative colitis (approximately 70%), Crohn disease (10% to 15%) and liver disease; peripheral blood eosinophilia is present in 90% of cases; some cases are idiopathic.

• Epithelial hyperplasia, spongiosis, and suprabasilar clefting with acantholysis are present; neutrophilic and eosinophilic abscesses are noted within the clefts and in the connective tissue papillae (Fig. 8-13).

• Direct immunofluorescence studies for immunoglobulin G (IgG) and C3 are negative.

• Pemphigus vulgaris exhibits intercellular deposition of IgG on direct immunofluorescence studies.

• Oral lesions respond well to topical steroids or tacrolimus (see Appendix A).

• Occurs in 1% to 2% of population, usually in adults

• Well-demarcated, patchy erythematous depapillation of tongue dorsum; raised, linear or circinate, often with discontinuous white peripheral rim; associated with fissured tongue in 25% of cases (Fig. 8-14, A and B); rare on sites other than the tongue (see Fig. 8-14, C)

• Loss of filiform papillae; psoriasiform epithelial hyperplasia with spongiosis and spongiotic pustules (involving one third to two thirds of the thickness of the epithelium); variable lymphocytic infiltrate (Figs. 8-15 to 8-17)

• Stains for candidal hyphae negative

• Candidiasis also shows psoriasiform epithelial hyperplasia and spongiotic pustules that are confined to the superficial two to three layers of keratinocytes; candidal hyphae are identified with periodic acid–Schiff stain.

• Spongiotic pustules at the edge of ulcers or in erosions involve the ulcer edge and the superficial keratinocytes.

• Condition is indistinguishable from psoriasis.

• Chronic resolving-relapsing condition

• Pain control with viscous lidocaine and diphenhydramine swish and spit preparation; topical steroids as necessary (see Appendix A)

• Painful erythematous lesions of the oral mucosa with symptoms coinciding with exposure

• Spongiotic mucositis with benign epithelial hyperplasia, variable chronic inflammation, and eosinophils in the lamina propria and epithelium (Fig. 8-18)

• Eosinophils and spongiosis seen in nonspecific inflammatory lesions

• Avoidance of inciting agent; topical steroids to resolve lesions (see Appendix A)