What is gum bleeding in systemic lupus erythematosus (SLE) and other autoimmune diseases, including its definition, pathophysiology, clinical manifestations, physical‑exam findings, and laboratory abnormalities?

Gum Bleeding in Systemic Lupus Erythematosus and Other Autoimmune Diseases

Definition

Gum bleeding in SLE and other autoimmune diseases primarily results from thrombocytopenia-induced hemorrhagic manifestations rather than direct gingival inflammation, though oral mucosal lesions are common in 75% of SLE patients. 1, 2

Gum bleeding represents a hemorrhagic complication of severe thrombocytopenia (platelet count <30,000/mm³) that occurs as part of the hematological manifestations of autoimmune disease, particularly SLE. 3

Pathophysiology

The mechanism of gum bleeding in autoimmune diseases involves multiple pathways:

• Autoimmune thrombocytopenia: Antiplatelet antibodies destroy platelets, leading to counts below the hemostatic threshold (<30,000/mm³), causing spontaneous mucosal bleeding including gingival hemorrhage. 3

• Interface mucositis: SLE causes direct oral mucosal damage through interface inflammation (not vasculitis, contrary to older theories), creating friable tissue prone to bleeding. 4

• Antiphospholipid antibodies: When present, aPL antibodies contribute to microvascular thrombosis and paradoxical bleeding through consumptive coagulopathy and thrombocytopenia. 3

• Complement-mediated tissue injury: Active complement consumption (low C3) correlates with disease activity and mucosal manifestations. 3

Notably, oral ulcerations do NOT result from necrotizing vasculitis as previously hypothesized—histological studies definitively show interface mucositis without leukocytoclastic vasculitis. 4

Clinical Manifestations

Oral Findings

• Spontaneous gingival bleeding: Occurs with platelet counts <30,000/mm³, presenting as oozing from gum margins without provocation. 3, 1

• Hemorrhagic oral bullae: Blood-filled blisters on oral mucosa represent severe thrombocytopenia and can be the presenting sign of SLE, particularly in pediatric patients. 1

• Oral ulcerations: Present in up to 75% of SLE patients, appearing as painful erosions on buccal mucosa, palate, or gingiva with erythematous borders. 5, 2

• Discoid lesions: Chronic, scarring plaques with central atrophy and peripheral erythema, occurring on oral mucosa in cutaneous lupus variants. 5

• Erythematous patches: Non-ulcerated red areas on oral mucosa representing acute cutaneous lupus involvement. 5

Systemic Manifestations Associated with Oral Bleeding

• Petechiae and purpura: Cutaneous hemorrhagic manifestations accompanying gingival bleeding when platelets <30,000/mm³. 3

• Active multisystem disease: Gum bleeding typically occurs during periods of generalized SLE activity affecting kidneys, joints, or other organs. 3

• Infection risk: Severe lymphopenia (<500 cells/mm³) and neutropenia (<500 cells/mm³) frequently accompany thrombocytopenia, increasing infection susceptibility. 6

Physical Examination Findings

Oral Cavity Examination

• Gingival hemorrhage: Spontaneous bleeding from gingival sulci or bleeding with minimal manipulation during examination. 1

• Hemorrhagic bullae: Tense, blood-filled blisters on any oral mucosal surface, which rupture leaving hemorrhagic erosions. 1

• Ulcer characteristics: Well-demarcated erosions with white-yellow fibrinous base and erythematous halo, typically on buccal mucosa or hard palate. 4, 2

• Poor oral hygiene: Difficulty maintaining oral care due to pain and bleeding, creating secondary periodontal issues. 2

Extraoral Findings

• Malar rash: Butterfly-shaped erythema across cheeks and nasal bridge, indicating active cutaneous SLE. 3

• Discoid lesions: Scarring, atrophic plaques on sun-exposed skin. 3

• Petechiae/purpura: Pinpoint hemorrhages or larger purpuric patches on skin and mucous membranes. 3

• Joint tenderness: Arthritis or arthralgias in multiple joints, particularly small joints of hands. 3

Laboratory Findings

Hematological Abnormalities

• Severe thrombocytopenia: Platelet count <30,000/mm³ requires immediate treatment; counts <50,000/mm³ indicate inadequate response to therapy. 3, 1

• Autoimmune hemolytic anemia (AIHA): Coombs-positive hemolytic anemia frequently accompanies thrombocytopenia in SLE. 3, 1

• Leukopenia: WBC <3.0 × 10⁹/L is common but rarely requires treatment unless severe neutropenia (<500 cells/mm³) develops. 3, 6

• Lymphopenia: Absolute lymphocyte count <500 cells/mm³ increases infection risk and warrants closer monitoring. 3, 6

Immunological Markers

• Positive ANA: Present in >95% of SLE patients, though not specific for disease activity. 1

• Anti-dsDNA antibodies: Correlate with disease activity and renal involvement; positive in patients with active SLE. 3, 1

• Anti-Smith antibodies: Highly specific for SLE diagnosis. 1

• Low complement levels: Decreased C3 and C4 indicate active disease and consumption through immune complex formation. 3

• Antiphospholipid antibodies: Present in subset of patients, associated with thrombotic complications and pregnancy morbidity. 3

Inflammatory Markers

• Normal or minimally elevated CRP: CRP typically remains <10 mg/L in active SLE; levels >50 mg/L strongly suggest superimposed bacterial infection rather than lupus activity alone. 3, 6, 7

• Elevated ESR: Non-specific marker of inflammation, typically elevated in active SLE. 3

Renal Function

• Urinalysis: Proteinuria, hematuria, and cellular casts indicate lupus nephritis, which frequently accompanies severe hematological manifestations. 3

• Serum creatinine: Elevated levels suggest renal involvement requiring aggressive immunosuppression. 3

• Urine protein/creatinine ratio: Quantifies proteinuria severity and guides treatment decisions. 3

Critical Clinical Pitfalls

• Do not attribute all gum bleeding to periodontal disease: In patients with known or suspected autoimmune disease, check complete blood count immediately to exclude life-threatening thrombocytopenia. 3, 1

• Do not assume elevated CRP indicates lupus flare: CRP >50 mg/L mandates workup for superimposed infection, as SLE characteristically produces minimal CRP elevation. 3, 6, 7

• Do not overlook drug-induced cytopenias: Immunosuppressive medications (azathioprine, mycophenolate, cyclophosphamide) commonly cause myelosuppression requiring dose adjustment or discontinuation. 3, 6

• Do not delay treatment of severe thrombocytopenia: Platelet counts <30,000/mm³ require immediate high-dose corticosteroids (intravenous methylprednisolone 1-3 days) combined with immunosuppressive agents to prevent life-threatening hemorrhage. 3