Premium
Cathepsin B‐ and L‐like activities at local gingival sites of chronic periodontitis patients
Author(s) -
Eley B. M.,
Cox S. W.
Publication year - 1991
Publication title -
journal of clinical periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.456
H-Index - 151
eISSN - 1600-051X
pISSN - 0303-6979
DOI - 10.1111/j.1600-051x.1991.tb00080.x
Subject(s) - connective tissue , periodontitis , cathepsin , chronic periodontitis , medicine , gingival and periodontal pocket , clinical attachment loss , pathology , gingivitis , cathepsin b , enzyme , chemistry , dentistry , biochemistry
The cysteine proteinases cathepsins B and L have the potential to degrade connective tissue in chronic periodontitis and this may progress episodically at individual tooth sites. The activities of cathepsin B‐ and L‐like proteinases in homogenised gingival tissue from control and periodontitis patients were measured biochemically using the selective peptide substrate Z‐Phe‐Arg‐AFC and the selective cathepsin L inhibitor Z‐Phe‐Phe‐CHN 2 . Each tooth site was divided, where appropriate, into gingival tissue and granulomata. These were assayed separately and the measurements related to the DNA and protein contents of the tissues. Enzyme activity in healthy control tissue was significantly lower than in diseased tissue. Enzyme activity in gingival tissue and total tissue from periodontitis patients decreased with increasing pocket depth, clinical attachment level, gingival index and bleeding index whilst cathepsin B activity in granulomata increased with increasing pocket depth and clinical attachment level but not with increasing gingival index or gingival bleeding index. Mean enzyme activity in gingival tissue was 1.6–2.8 times greater than in granulomata. Mean patient enzyme activity in diseased patients did not correlate positively with their mean pocket depth, clinical attachment level, gingival index or gingival bleeding index. These results are best explained by the probable cellular origins of the enzymes and the likely influence of their serum and tissue inhibitors during the disease process.