Project: Research project

Project Details


There is general agreement in the literature that the
polymorphonuclear leukocyte (PMN) is the prominant cell type
during all phases of periodontal health and disease. The
importance of the PMN in the maintenance of periodontal health
is suggested by the severe inflammation and periodontal
destruction observed in patients with systemic PMN defects. The
exact role for PMNs on a cellular basis is not will understood.
They are considered to be protective against infection and exert
this function presumably by phagocytosis, antibody dependent
killing, and release of antimicrobial substances. Despite the
association between neutrophil defects and severe periodontal
disease, no clear association between neutrophil dysfunction and
susceptibility has been established for Advanced Adult
Periodontitis (A.A.P.), a chronic disease characterized by severe,
generalized inflammation, bone loss and early tooth loss.
Bacteriodes gingivalis has been implicated as an etiologic agent of
A.A.P. Based on the current literature, it is not clear what role
PMNs play in defense against B. gingivalis. It is possible that
there may be subtle neutrophil dysfunction in dealing with this
pathogen, associated with susceptibility to A.A.P. The proposed
studies are therefore intended to begin to define the nature of the
PMN interaction with B. gingivalis. Initial studies will examine
the ability of peripheral blood neutrophil from normal patients to
phagocytize and kill B. gingivalis. The role of antibody (and
complement) in this process will be defined, and further
characterized by an enzyme linked immunoadsorbent assay
(ELISA) utilizing patient sera and killed B. gingivalis organisms to
determine responsible isotypes. Antigen specificity will be
elucidated by SDS-PAGE and trans-immunoblotting. The possible
involvement of oxygen dependent mechanisms of killing of B.
gingivalis by neurtophils will be determined and may involve
myeloperoxidase (MPO), lactoferrin (LF), H202, hydroxy radical,
singlet oxygen and superoxide production, and may occur
intracellularly and extracellularly. Non-oxygen dependent
mechanisms, involving lysozyme, lactoferrin, cationic proteins
and small peptides will also be examined and may be contributory.
Although nothing in the literature suggests any innate defect in
A.A.P. patient neurtorphils, most studies used unrelated bacteria
at test organisms. Phase II will focus on comparing the abilities
of normal and patient neutorphils to phagocytize and kill B.
gingivalis, while examining degranulation, superoxide production
and chemotaxis to complete this profile.
StatusNot started


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