Porphyromonas gingivalis lipopolysaccharide activated bone resorption of osteoclasts by inducing IL-1, TNF, and PGE.
OBJECTIVE
To study the effects of Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) on inducing interleukin-1 (IL-1), tumor necrosis factor (TNF), prostaglandin E (PGE), and activating osteoclasts, in order to understand mechanism of osteoclast activation.


METHODS
Pg-LPS was prepared by phenol-water method. IL-1, TNF, and PGE induced by Pg-LPS were isolated by chromatography. Ca2+ concentration was detected by atomic absorption spectrophotometry. Acid phosphatase and carbonic anhydrase in periodontal membranes were examined by histochemistry.


RESULTS
Pg-LPS was able to stimulate peripheral blood mononuclear cells (PBMC) or the cells from human periodontal tissue secreting IL-1, TNF, and PGE. The outputs of these cytokines were increased in pace with the enhancement of Pg-LPS at the dose range of 0.5 - 5.0 mg/L. All of the three cytokines showed activities of accelerating Ca2+ release from rat calvarial bones, and the activity of PGE was the strongest. The amounts of both the acid phosphatase and carbonic anhydrase in the periodontal membranes of Pg-LPS injected rats were obviously increased (P < 0.01). In the periodontal membranes of Pg-LPS injected rats, the amount of activated osteoclasts were obviously increased in pace with Pg-LPS injection times (P < 0.01). However, the activating rates of osteoclasts were stable to approximately 65 % because of the increase of inactivated osteoclasts.


CONCLUSIONS
Pg-LPS possessed strong activities to induce human PBMC and the cells from human periodontal tissue to produce IL-1, TNF, and PGE in a dose-dependent m anner within a certain concentration range of the LPS. Pg-LPS could efficiently activate osteoclasts, and the mechanism of osteoclast activation was probably associated with the increase of acid phosphatase and carbonic anhydrase.
Chen
L L
LL
Department of Stomatology, the Second Affiliated Hospital, Medical School of Zhejiang University, Hangzhou 310009, China.
Yan
J
J
D000527:Alprostadil / Q000096:biosynthesis; D000818:Animals; D000831:Animals, Newborn; D001862:Bone Resorption; D005881:Gingiva / Q000166:cytology; D006801:Humans; D007375:Interleukin-1 / Q000096:biosynthesis*; D007963:Leukocytes, Mononuclear / Q000166:cytology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D010010:Osteoclasts / Q000166:cytology / Q000378:metabolism*; D010519:Periodontium / Q000166:cytology; D016966:Porphyromonas gingivalis / Q000302:isolation & purification; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D000527:Alprostadil