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Matrix metalloproteinase 2 (MMP-2) has been implicated to play a role in pathogenesis of periodontal disease. We recently reported thatPorphyromonas gingivalissupernatant could activate MMP-2 in human periodontal ligament (HPDL) cells. In this study, activation of MMP-2 byActinobacillus actinomycetemcomitanssupernatant and the mechanism was investigated.HPDL cells were treated with eitherA. actinomycetemcomitansorP. gingivalissupernatant for 48 h. To verify the mechanism, pretreated inhibitors were used. Gelatin zymography, RT-PCR and Western blot analysis were used to detect the activation of MMP-2, expression of MT1-MMP and TIMP-2 mRNA and the proteins, respectively.The supernatant fromA. actinomycetemcomitanscould activate MMP-2 in HPDL cells similar to that fromP. gingivalisbut by a different mechanism. Activation byA. actinomycetemcomitanssupernatant was correlated with a reduction of TIMP-2 secretion without any alteration of MT1-MMP, while activation byP. gingivalisincreased MT1-MMP but no change of TIMP-2 was found.The supernatant fromA. actinomycetemcomitansandP. gingivaliscould induce the activation of MMP-2 possibly through the imbalance of MT1-MMP and TIMP-2 in HPDL cells but by different mechanisms. The imbalance of MT1-MMP and TIMP-2 may be another factor that is involved in the severity of periodontal disease. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to determine the timing of colonization of streptococci mutans (SM) in 2- to 36-month-old Thai children.Methods: Two hundred and two 2- to 36-month-old children were divided into 3 groups: group 1 = 84 predentate children; group 2 = 68 children with 1 to 8 erupted teeth; and group 3 = 50 children with 9 to 20 erupted teeth. Microbiological samples were obtained from children by cotton swab. Samples were diluted and plated on mitis salivarius agar supplemented with Baocitracin (MSB) for selection and enumeration of SM.Results: SM colonization was found in 26% of children, who had a mean age in months of 20.5 +/- 103 (SD). MS colonization was detected in 5% of predentate children and was detected in children as young as 2 months old. The percentage of children who were colonized with SM rose significantly with increasing age and numbers of erupted teeth (P < .001).Conclusions: Streptococci mutans colonization in 2- to 36-month-old Thai children was found in predentate children and detected in children as young as 2 months old. The results suggest that prevention of early SM colonization in some populations may need to be initiated prior to tooth eruption. [ABSTRACT FROM AUTHOR]

Background: The lipopolysaccharide (LPS) of A. actinomycetemcomitans is one of the major pathogenic factors in periodontal disease. It induces secretion of proinflammatory cytokines and is involved in alveolar bone destruction. We hypothesized that the LPS of A. actinomycetemcomitans could affect the activation of matrix metalloproteinase (MMP)-2 and the expression of receptor activator of nuclear factor kappa B ligand (RANKL) and osteoprotegerin in human periodontal ligament (HPDL) cells leading to the destruction of periodontium., Methods: HPDL cells were cultured in serum-free medium with or without the LPS of A. actinomycetemcomitans for 36 hours. The activation of MMP-2 was analyzed by zymography. Changes of the expression of RANKL and osteoprotegerin (OPG) were examined by reverse transcription-polymerase chain reaction and supported by Western blot analysis., Results: The activation of MMP-2 could be induced by the LPS of A. actinomycetemcomitans in HPDL cells and could be inhibited by a serine protease inhibitor. This result suggested that the LPS might activate MMP-2 through a serine protease-dependent pathway. This activation was also blocked by NF-kappaB inhibitor, which indicated the involvement of NF-kappaB. The upregulation of RANKL but not OPG by the LPS was found in both transcription and translation and could be reduced by indomethacin. In addition, serine protease inhibitor also inhibited the upregulation of RANKL, suggesting the activity of serine protease., Conclusions: The effect of the LPS of A. actinomycetemcomitans on HPDL cells is serum-independent and the induction of the activation of MMP-2 and the expression of RANKL are serine protease-dependent pathways. The results suggest the role of HPDL cells in the pathogenesis of periodontitis.

It has been reported that matrix metalloproteinase (MMP) produced by host cells plays a major role in periodontal tissue destruction. In addition, secreted virulence factors from Porphyromonas gingivalis can alter MMP secretion and cause activation in host cells that lead to the tissue degradation. In this study, we examine the effects of P. gingivalis supernatant on matrix metalloproteinase-2 (MMP-2) activation in human periodontal ligament (HPDL) cells. Cultures of HPDL cells were treated with P. gingivalis supernatant for 48 h and the level of MMP-2 activation was monitored by gelatin zymography. The profound activation of MMP-2 was seen only in the treated group. The activation of MMP-2 was inhibited by MMP inhibitors phenanthroline and EDTA, but not serine protease or cysteine protease inhibitors. To study the correlation between the expression of membrane-type-1 matrix metalloproteinase (MT1-MMP) and the activation of MMP-2, the level of MT1-MMP was analyzed. The results from reverse-transcription polymerase chain reaction (RT-PCR) and Western analysis indicated that P. gingivalis supernatant up-regulated the expression of MT1-MMP in both transcription and translation levels within 48 h. These results suggest that P. gingivalis supernatant can activate MMP-2 in HPDL cells and the mechanism of activation may involve the increased amount of MT1-MMP. It is possible that the activation of MMP-2 by P. gingivalis plays a role in the process of chronic periodontitis.