Host Response in Chronic Periodontal Disease: V. The Dental and Periodontal Status of Mink and Mice Affected by Chediak‐Higashi Syndrome

Abstract

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...

Experimental Animal Models in Periodontology: A Review

“…In the lower jaw, the amount of attached gingiva is narrow in the incisors and premolars. Around the molars, attached gingiva appeared to be comparable to that observed in the upper jaw [106]. In CSH-affected minks, periodontal disease occurs rapidly with a high hemorrhagic inflammatory response in the marginal gingiva.…”

The genetic basis of periodontitis

“…Those affected are very susceptible to bacterial infections due to alterations in the functional capacity of the polymorphonuclear leukocyte. Humans (59) and other animals (105) with Chediak–Higashi syndrome exhibit generalized, severe gingivitis and extensive loss of alveolar bone and premature loss of teeth (168). The polymorphonuclear leukocyte chemotactic and bactericidal functions are thought to be abnormal in these patients.…”

Gingivitis and oral ulceration in patients with neutrophil dysfunction

“…Polymorphonuelear neutrophils are an essential part of host defense against invading bacteria (1). Several studies have shown that periodontal diseases in man (2)(3)(4)(5) and in animal (6) arc associated with defective neutrophil function, providing support lor the concept that neutrophils are protective against pathogenic oral bacteria. In addition, several studies have shown that crcvicular neutrophils function better in vitro when they are recovered from healthy compared with diseased gingival pockets (7).…”