Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031099 (periodontitis)
 12,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent research evidence shows that the receptor activator of nuclear factor-kappa B ligand (RANKL) and osteoprotegerin (OPG) play an important role in osteoclastogenesis and the inflammatory bone loss during periodontitis. Bone remodeling process is dependent on the balance of these two proteins while a high ratio of RANKL/OPG characterizes the increased osteolytic process and it has been reported in inflammatory diseases including the periodontal disease. The purpose of this study was to determine the OPG and RANKL mRNA levels in periodontal tissues derived from patients with advanced chronic periodontitis after non-surgical periodontal therapy (SRP) and to compare the RANKL/OPG ration with that in healthy persons. Gingival biopsies were obtained from subjects with clinically healthy periodontium (H) (N = 11) and patients with advanced chronic periodontitis (CP) (N = 14). Total RNA was isolated from the gingival samples and 1 microg RNA was reverse transcribed to cDNA, followed by polymerase chain reaction (PCR) using specific primers for OPG and RANKL. The efficiency of reverse transcription was verified by the amplification of the GAPDH gene. The intensity of RT-PCR products was analyzed by a densitometer and was normalized to the intensity of the band for the housekeeping gene GAPDH. Immunohistochemical evaluation of the RANKL and OPG expression was also performed. The expression of RANKL as well as of OPG was reduced in CP specimens in comparison to that of healthy persons in a statistical significant way. However, the RANKL/OPG ratio showed to be slightly elevated in CP compared to H specimens but this finding was not of statistical significance. The immunohistochemical analysis revealed a non-uniform expression pattern for both proteins. Although further investigation is needed to identify the specific role of RANKL and OPG protein in periodontitis progression, our data after SRP might indicate the possible involvement of these proteins in the activation of pathways, which regulate the repair of the periodontal tissues.
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PMID:RANKL and OPG mRNA level after non-surgical periodontal treatment. 2003 78

The up-regulation of the B7-H1 receptors in host cells might influence the chronicity of inflammatory disorders that frequently precede the development of human cancers. B7-H1 expression has been detected in the majority of human cancers, leading to anergy and apoptosis of activated T cells, and enabling tumor cells to overcome host response. Porphyromonas gingivalis (P. gingivalis), a putative periodontal pathogen, is an etiologic agent of periodontitis and expresses a variety of virulence factors. In this study, the expression of B7-H1 and B7-DC receptors on squamous cell carcinoma cells SCC-25 and BHY and primary human gingival keratinocytes (PHGK) was analyzed after infection with two virulent P. gingivalis strains in vitro. After 48h, the cells were stained with antibodies for human B7-H1 and B7-DC and further analyzed by flow cytometry. RNA was extracted and gene expression of B7-H1 or B7-DC was quantified by real time PCR. After infection with P. gingivalis, both B7-H1 and B7-DC receptors were up-regulated. The mean fluorescence intensity (MFI) increased from 4.5 to 9.9 (B7-H1) and from 6.9 to 15.0 (B7-DC) (p<0.05, respectively) in SCC-25 cells. PHGK showed an increase from 4.8 to 12.4 (B7-H1) and from 5.5 to 15.6 (B7-DC) (p<0.05, respectively). Streptococcus salivarius K12, a commensal bacterium, caused no up-regulation. After 24h, the expression of B7H1 and B7-DC mRNA in infected cells, normalized to GAPDH and in relation to non-infected cells, was 6.4 fold (B7-H1) and 8.6 fold (B7-DC) higher. In PHGK B7-H1/DC mRNA expression increased 8.2 fold (B7-H1) and 5.9 fold (B7DC) (p<0.05) respectively. The results of the study demonstrate that in contrast to S. salivarius K12 virulent P. gingivalis strains are able to induce the expression of the B7-H1 and B7-DC receptors in squamous carcinoma cells and human gingival keratinocytes, which might facilitate immune evasion by oral cancers.
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PMID:B7-H1 and B7-DC receptors of oral squamous carcinoma cells are upregulated by Porphyromonas gingivalis. 2172 42