Pm. Loomer et al., DIRECT EFFECTS OF METABOLIC PRODUCTS AND SONICATED EXTRACTS OF PORPHYROMONAS-GINGIVALIS-2561 ON OSTEOGENESIS IN-VITRO, Infection and immunity, 62(4), 1994, pp. 1289-1297
It is well documented that oral microorganisms play a significant role
in the initiation and progression of periodontal disease. By using va
rious in vitro models, it has been shown that some bacteria considered
periodontal pathogens or their products can Stimulate bone resorption
and some other parameters of osteoblast-like cell activity. However,
the effects of these organisms and their products on osteogenesis itse
lf are not known. This study was undertaken to determine the direct ef
fects of metabolic products and sonicated extracts of Porphyromonas gi
ngivalis on bone formation in the chick periosteal osteogenesis model.
Cultures of P. gingivalis 2561 were grown under standard anaerobic cu
lture conditions. The spent medium was collected, and following centri
fugation, sonicated bacterial extracts were prepared from the bacteria
l pellet. These were added in various proportions to the chick periost
eal osteogenesis cultures. Sonicated extracts were further fractionate
d into five molecular-size ranges and similarly tested. Parameters of
osteogenesis, including alkaline phosphatase activity, calcium and P-i
accumulation, and collagen synthesis, were measured on 6-day-old cult
ures. Compared with controls devoid of bacterial products, osteogenesi
s was inhibited significantly in cultures treated with either conditio
ned medium or extracts obtained from P. gingivalis. Various amounts of
inhibitory activity were observed in the different ultrafiltration mo
lecular-size fractions, with very profound inhibitory effects observed
in the <5-kDa range. Histological observations indicated the presence
of cells, some bone, and/or new fibrous connective tissue at all conc
entrations, indicating that toxicity was not a factor. These results s
uggest that periodontal pathogens such as P. gingivalis might contribu
te to the bone loss in periodontal diseases not-only by stimulating re
sorption but, possibly, by inhibiting bone formation directly.