Polymorphonuclear leukocyte chemotactic studies were performed in young patients with juvenile periodontitis/periodontosis and adult patients with aggressive periodontitis. In the juvenile periodontitis/periodontosis group, 86% showed modest leukotactic defects, the majority of which were due to intrinsic abnormality of cells. In the older patients with rapidly progressing periodontitis 48% had detectable leukotactic defects; the majority of which were serum associated. The results indicate that some forms of periodontitis are associated with impaired polymorphonuclear leukocyte chemotaxis and suggest that a failure of a major host protective mechanism to dental plaque may increase susceptibility to periodontal disease.

IN BOTH HUMANS and animals, the accumulation of microbial plaque leads to the infiltration of large numbers of neutrophils within the marginal gingival tissues at a time prior to the appearance of lymphoid cells. 16 The appearance of these cells is accompanied by loss of a large portion of the collagen fibers immediately subjacent to the junctional epithelium. 4 6 Neutrophils have the capacity to ingest and kill microorganisms and they may be predominantly protective, although it has been suggested that they may participate in the observed tissue damage. 7-9 For example, neutrophils carry a wide variety of hydrolytic enzymes including collagenase which may be released following their encounter with either bacteria or immune complex. The role these cells play in inflammatory gingival and periodontal disease has not been elucidated. Analysis of the dental and periodontal status of animals and humans with defects in polymorphonuclear leukocyte function such as in the Chediak-Higashi syndrome may help elucidate the role of these cells in the disease. The Chediak-Higashi syndrome (C-HS) is a genetically transmitted autosomal recessive trait identified in humans, cattle, mink and mice. Affected individuals and animals are unusually susceptible to bacterial infections and this enhanced susceptibility may be related to alteration in the functional capacity of the blood leukocytes. In addition, C-HS mink are more susceptible than unaffected mink to Aleutian disease, a slowly progressive debilitating viral infection characterized by widespread proliferation of plasma cells and lymphocytes, hyper-gammaglobulinemia, glomerulonephritis and necrotizing arteritis. 40 One characteristic of C-HS is the presence of abnormally large lysosomes in the neutrophilic leukocytes and abnormal neutrophil function. If polymorphonuclear leukocytes contribute significantly, either defensively or offensively, to the host response to microbial plaque accumulation, the prevalence and severity, and possibly the morphology, of periodontal disease in affected and nonaffected individuals and animals would be expected to differ. We report qualitative and quantitative clinical and histopathologic features of inflammatory periodontal disease in normal mink and mice and in those carrying the C-HS trait. EXPERIMENTAL METHODS Female mink (Mustella vison), ranging in age from 3 to 5 years and free of clinical signs of Aleutian disease, were obtained from the breeding stock of local mink ranchers, were housed individually in the vivarium of the University of Washington for time periods up to 6 months and fed a commercially available diet (Northwest Fur Breeders, Edmonds, Wash.). Twelve normal animals and 12 animals carrying the Chediak-Higashi syndrome (C-HS) trait were studied. In addition, the heads of six each of C-HS and normal animals 6 months of age and 18 months of age were obtained and studied. Subsequently the skulls of six mice (C57BL/6Jbg) homozygous for the beige trait (C-HS), and six mice heterozygous for the same trait, all 1 year of age, were...

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