This review presents evidence for lysosomal enzymes being at least partly responsible for the tissue destruction seen in periodontal disease. However, many other inflammatory and immunologic mechanisms have been identified that can contribute to tissue destruction (Nisengard 1977). The relationship of PMN to the periodontal tissues is equivalent to the proverbial double-edged sword. The localized tissue destruction that may be due to the extracellular release of PMN enzymes in individuals with normal cell function must be weighed against the role of PMN in containment of gingival bacteria and their products. The consequences of qualitative and/or quantitative abnormalities of neutrophils are far more undesirable for the periodontium. It therefore seems logical to propose that the role of polymorphonuclear leukocytes in the gingival tissues is primarily a defensive one. The presence of neutrophils in the gingival crevice has been shown to reflect the inflammatory condition of the tissues. Due to their availability, it may prove beneficial to use gingival crevicular PMN activity as a reliable clinical index of disease activity. The development of appropriate tests to measure PMN may eventually lead to better diagnostic criteria, including the definition of active versus inactive disease.

The frequency of HL-A2 was significantly low (21%) in patients with periodontitis when compared to controls who were free of periodontal disease (61%). The effect was most pronounced in females in whom HL-A2 was present in 12.5% (2 out of 16). This finding suggests that genes controlling susceptibility to microbial agents may be linked to the HL-A LOCUS.

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