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Introduction: Granulomatosis with polyangiitis (GPA), formerly known as Wegener granulomatosis, is a multisystem disorder that mainly involves airways and kidneys. Oral GPA may present as ulcerations or strawberry gingivitis. Early diagnosis and intervention are crucial for overall prognosis.Case Presentation: An unusual case of oral GPA manifested by chronic localized inflammation, leading to failure of dental implants in an elderly woman, is presented. Diagnosis was based on antineutrophil cytoplasmic testing and histopathologic evidence of necrotizing vasculitis. Disease remission was achieved with cyclophosphamide and steroids.Conclusion: Familiarity with oral manifestations of GPA will help dentists and oral surgeons diagnose and treat early or incipient GPA without delay.

Systemic lupus erythematosus (SLE) is a systemic inflammatory disease characterized by autoantibody production and immune complex tissue deposition. The clinical picture of lupus varies from mild skin lesions to severe organ damage, such as glomerulonephritis that may ultimately result in end stage renal disease. Inflammatory illnesses such as lupus are characterized by an aberrant cytokine profile; the balance of pro- and anti-inflammatory cytokines is tipped towards inflammation. Interleukin-10 (IL-10) plays a key role in maintaining this balance, as it blocks inflammatory cytokine synthesis (1), chemokine secretion (2), inflammatory enzyme production and expression of co-stimulatory molecules including CD80, CD86 and MHC Class II (3). To limit inflammation, IL-10 also promotes production of IL-1 receptor antagonists and soluble TNFα receptors (1). In certain cases, however, IL-10 exerts immunostimulatory effects, acting as a potent cofactor for proliferation, differentiation, class switching, and antibody production in B lymphocytes (1). IL-10 is among the cytokines thought to be dysregulated in SLE. Serum IL-10 levels are elevated in SLE patients and the extent of elevation correlates with disease activity (4). Polymorphisms within the IL-10 gene promoter that are associated with high IL-10 levels may be important in the development of certain clinical features in SLE (5,6). Monocytes and B lymphocytes from SLE patients spontaneously produce high amounts of IL-10 in vitro (7,8) Cells from healthy relatives of SLE patients also produce increased amounts of IL-10 (9), suggesting that IL-10 may be a pathogenic factor in lupus. Indeed, immunoglobulin production by B lymphocytes in SLE is in part IL-10 dependent (10), and, in one small human trial, anti-IL-10 monoclonal antibody therapy was shown to be beneficial for SLE patients with active, steroid-dependent disease (11). SLE is characterized by increased production and decreased clearance of immune complexes. In SLE, immune complexes mediate tissue damage by cross-linking myeloid cell surface Fcγ recptors (FcγRs), thereby activating cellular effector functions, including phagocytosis of pathogens, endocytosis of immune complexes, and production of cytokines, chemokines and reactive oxygen intermediates (12–15). In the presence of IgG-containing immune complexes, macrophages produce high levels of IL-10, which can dampen innate inflammatory responses to microbial infections (16), or, in lupus patients, affect the autoimmune response. Previous studies have shown that IL-10 activity is suppressed at the level of Jak-Stat signal transduction when FcγRs are crosslinked by immune complexes in IFNγ-primed macrophages (17). Given paradoxically high levels of IL-10 and the abundance of immune complexes in SLE patients, we hypothesize that the anti-inflammatory function of IL-10 is limited in SLE monocytes, leading to unrestrained monocyte activation at sites of immune complex deposition.