No abstract

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.

Genistein and other inhibitors of protein tyrosine kinases were examined for effects on neurite elongation and growth cone morphology in the rat PC12 pheochromocytoma cell line. Genistein increased the rate of neurite elongation in PC12 cells grown on a collagen/polylysine substratum after priming with nerve growth factor (NGF), but had no effect on undifferentiated cells. Steady-state levels of phosphotyrosine-modified proteins (105, 59, 52, and 46 kDa) were reduced in NGF-primed cells by genistein treatment. The target of genistein action did not appear to be the NGF receptor/trk tyrosine kinase because the presence of NGF in cultures of NGF-primed cells was not necessary for genistein-stimulated neurite outgrowth. The tyrosine kinase inhibitors tyrphostin RG508964 and herbimycin A also increased the rate of neurite elongation in NGF-primed PC12 cells. Video-enhanced differential interference contrast microscopy revealed that growth cones of genistein-treated cells had less complex morphologies and were less dynamic than untreated cells, with short filopodia restricted to the leading edge, unlike untreated cells whose growth cones exhibited longer, more numerous filopodia and lamellipodia, which remodeled continuously. These results suggest that protein tyrosine kinase activity in PC12 cells negatively regulates neurite outgrowth and directly or indirectly affects growth cone morphology.

Advances in periodontics with respect to disease activity, microbiology and immunology have demonstrated the multifactorial nature of periodontal diseases. This serves to underscore the need for an ideal animal model for periodontal research. Non-human primates are most similar to man in comparison to other animal models. The baboon is an Old World monkey that has infrequently been used in periodontal research. Periodontal exams were accomplished on 116 baboons (Papio anubis, P. cynocephalus) ages 5 to 30 years with one baboon year being roughly equivalent to 3 to 4 human years. The study population consisted of 29 males and 87 females. Clinical parameters including probing depth, attachment level, mobility, plaque index and gingival index were collected. Radiographs were taken on 25 animals and correlated to clinical findings. Results showed a significant increase in mean probing depth and mean attachment level with age (p = 0.0001). Disease prevalence and severity were not significantly different between genders. Mobility was uncommon; however, the prevalence and severity of furcation involvement increased with age. Radiographs suggested horizontal and isolated vertical bone loss. Plaque and gingival indices were at sustained high levels for all age groups and showed a statistically significant increase with age. Some baboons were found to develop a naturally-occurring periodontitis that increased in severity with age. This primate may be a suitable model for studies in human periodontal disease.