Histochemical study of periodontitis in MRL/* mice with immunological disorder

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The unequivocal main cause of periodontitis is bacterial plaque present in the gingival sulcus, and it is widely accepted that Gram-negative anaerobic rods in dental plaque are essentially responsible for the onset and progression of this disease. In addition however, there are many other factors, local and systemic, that effect the onset and progression of periodontitis. Systemic factors include nutritional deficiency, metabolic disturbance, endocrinopathy, allergy, and autoimmune diseases. In the latter case, vasculitis is often evident, and its presence in periodontal tissue is thought to result in more severe tissue destruction. In order to elucidate this process, periodontitis was induced by ligature in MRL/MPJ-lpr/lpr mice with autoimmune disease, and studied histochemically. The gingival sulcular epithelium (GSE) became ulcerated and polymorphonuclear leukocytes (PMNs) were found to infiltrate the GSE. Macrophages, lymphocytes and PMNs were observed beneath the GSE and junctional epithelium (JE). The PMNs were ultrastructurally evident in the intercellular spaces of the epithelium, and PMNs, macrophages with large dense bodies and lymphocytes also were seen adjacent to the GSE and JE. The 1-positive were observable immunohistochemically in and beneath the GSE and JE. Cells with intense acid phosphatase activity accumulated beneath the GSE and JE. These cells were considered to be macrophages. This cellular accumulation beneath the GSE and JE indicates that the destruction of periodontal tissue due to inflammation is exacerbated by the coexistence of vasculitis.