Date of Award

Spring 1997

Document Type

Thesis - Restricted

Degree Name

Master of Science (MS)



First Advisor

Dentino, Andrew R.

Second Advisor

Ellinger, Royal

Third Advisor

Van Swol, Ronald


The observation that the majority of refractory periodontitis cases occur in habitual smokers, has kindled interest in examining the effects of smoking, and specifically nicotine, on those cells which make up and protect the periodontium. It has recently been reported that diseased matched periodontal pockets in smokers and non smokers are very similar with regard to the prevalence of the major periodontopathic bacteria. These findings are consistent with the possibility that the progressive breakdown of the dentoalveolar complex in smokers may result from alterations in host defense, rather than specific pathogenic shifts in the microecology of the periodontal pocket. Neutrophils (PMNs) are the predominant leukocytes in the gingival pocket epithelium and the adjacent connective tissue. These cells play a protective role in the periodontium and patients with severe quantitative or qualitative defects may be predisposed to periodontal diseases. Aggressive forms of periodontal disease studied to date, in general, have shown alterations involving PMN functions which are dependent on adhesive interactions. In particular several lines of evidence implicate alterations in neutrophil chemotaxis and/or adherence as major risk factors for periodontal breakdown. Adhesion of PMNs to endothelial cells is an early and requisite event in acute inflammation. The three families of adhesion molecules that participate in this process are the selectins namely L-selectin, the immunoglobulin superfamily which includes intercellular and vascular cell adhesion molecules and the integrins namely Mac-1. A two step adhesion model for neutrophil interaction with endothelium has been proposed based on the observation that Mac-1 and L-selectin are inversely regulated by exposure to chemotactic factors. The down regulation of L-selectin and up regulation of Mac-1 suggests that these adhesion molecules mediate distinct and complimentary adhesion events. The present study aims to gain information on the neutrophil adhesion protein phenotype in smokers and non smokers, with and without periodontal disease. A cross sectional survey was performed with a p redetermined patient population of smokers and non smokers with and without periodontal disease. Protein receptor expression was quantified to determine whether chronic inflammatory periodontal disease activity and or smoking is associated with altered protein receptor expression of adhesion molecules Mac-I and L-selectin on the cell membrane of the neutrophil.



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