Simultaneous assessment of complement components C3, C4, and B and their cleavage products in human gingival fluid: II. Longitudinal changes during periodontal …

CE Niekrash, MR Patters - Journal of periodontal research, 1985 - Wiley Online Library
CE Niekrash, MR Patters
Journal of periodontal research, 1985Wiley Online Library
The activation of the complement system is an important host‐mediated mechanism in the
initiation and progression of inflammation. Complement cleavage products have been
reported in gingival fluid obtained from periodontitis lesions suggesting a potential role for
the activation of the alternative and/or classical complement pathways in the pathogenesis
of periodontitis. Using the multi‐layer crossed immunoelectrophoresis technique, the effect
of periodontal therapy on complement conversion of C3, C4, and B was assessed in 37 sites …
The activation of the complement system is an important host‐mediated mechanism in the initiation and progression of inflammation. Complement cleavage products have been reported in gingival fluid obtained from periodontitis lesions suggesting a potential role for the activation of the alternative and/or classical complement pathways in the pathogenesis of periodontitis. Using the multi‐layer crossed immunoelectrophoresis technique, the effect of periodontal therapy on complement conversion of C3, C4, and B was assessed in 37 sites in 9 patients. Patients selected for study had moderate‐severe periodontitis as confirmed by clinical measurements of plaque, gingival inflammation, bleeding on probing, suppuration, pocket depth, and loss of attachment. Gingival fluid and clinical indices were obtained from representative sites prior to treatment and again 2–4 weeks following extensive periodontal scaling and root planing.
Periodontal therapy resulted in a statistically significant decrease in all clinical parameters of inflammation. The percentage of C3 conversion decreased significantly from 70.0% to 37.5% with therapy (p=0.0001) while the reference protein, transferrin, did not significantly change. C4 conversion to C4c was never observed and total C4 was not significantly altered by therapy. Changes in B conversion to Bb could not be evaluated because the Bb precipitate was too small to measure reproducibly. These results suggested that complement activation, as measured by C3 conversion to C3c, decreased in gingival fluid following periodontal therapy and suggested a role for complement activation in the pathogenesis of inflammatory periodontal disease.
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