MATERIALS AND METHODS: The addressed focused question was "Is there a difference in the resistin levels between individuals with CP and those without CP?" four electronic databases: Medline, PubMed (National Institutes of Health, Bethesda), EMBASE, and Science direct databases from 1977 up to March 2016 for appropriate articles addressing the focused question. EMBASE and Medline were accessed using OVID interface which facilitated simultaneous search of text words, MeSH or Emtree. Unpublished studies (gray literature) were identified by searching the Open-GRAY database and references of the included studies (cross referencing) were performed to obtain new studies. In-vitro studies, animal studies, studies that reported levels of other cytokines but not resistin, letters to the editor and review papers were excluded.
RESULTS: Ten studies were included. Nine studies compared resistin levels between CP and periodontally healthy (H) individuals and reported higher mean serum and GCF levels of resistin in CP patients than the H controls. Two studies showed comparable resistin levels from GCF and serum between diabetes mellitus with CP (DMCP) and CP groups. Three studies included obese subjects and showed comparable serum and GCF resistin levels between obese subjects with CP (OBCP) and CP subjects.
CONCLUSIONS: CP patients were presented with elevated levels of GCF or serum resistin as compared with H individuals. Resistin modulates inflammation in chronic periodontal disease and may be used as surrogate measure to identify subjects at risk for periodontitis. Resistin levels in patients with CP and systemic inflammatory disorders such as diabetes, obesity, or rheumatoid arthritis was not significantly higher than the levels in patients with only CP.
METHOD: Subjects were allocated into RA (n = 49) or non-RA (NRA) (n = 55) groups, where 3 subgroups were further established; chronic periodontitis (CP), gingivitis (G) and periodontal health (H). Demographic and periodontal parameters were collected. Rheumatology data were obtained from hospital records. Serum and salivary LL-37 levels were measured using enzyme-linked immunosorbent assay and compared for all groups.
RESULTS: For salivary LL-37, RA-CP was significantly higher than NRA-G and NRA-H (P = .047). For serum LL-37, all RA and NRA-CP were significantly higher than NRA-G and NRA-H (P = .024). Salivary LL-37 correlated negatively with clinical attachment loss (CAL) (P = .048), but positively with erythrocyte sedimentation rate (ESR) in RA-H (P = .045). Serum LL-37 showed positive correlation with ESR (P = .037) in RA-G, with C-reactive protein (P = .017) in RA-H, but negative correlation with number of teeth (P = .002) in NRA-CP. Rheumatology data correlated positively with periodontal parameters in RA-CP group.
CONCLUSION: NRA-CP subjects with high serum LL-37 should receive comprehensive periodontal therapy. Positive correlation between rheumatology data and periodontal parameters showed that RA disease stability may be obtained by assessing the periodontal condition. Periodontal therapy is necessary to compliment RA treatment to achieve optimum outcome for RA patients with concurrent CP.
MATERIAL AND METHODS: Using an Oragene® RNA kit, the total RNA was purified from the saliva of 10 patients with chronic periodontitis and 10 patients without chronic periodontitis. The quantity and quality of the total RNA was determined, and a measure of gene expression via cDNA was undertaken using the Affymetrix microarray system. The microarray profiling result was further validated by real-time quantitative polymerase chain reaction.
RESULTS: Spectrophotometric analysis showed the total RNA purified from each participant ranged from 0.92 μg/500 μL to 62.85 μg/500 μL. There was great variability in the quantity of total RNA obtained from the 2 groups in the study with a mean of 10.21 ± 12.71 μg/500 μL for the periodontitis group and 15.97 ± 23.47 μg/500 μL for the control group. Further the RNA purity (based on the A260 /A280 ratio) for the majority of participants (9 periodontitis and 6 controls) were within the acceptable limits for downstream analysis (2.0 ± 0.1). The study samples, showed 2 distinct bands at 23S (3800 bp) and 16S (1500 bp) characteristic of bacterial rRNA. Preliminary microarray analysis was performed for 4 samples (P2, P6, H5 and H9). The percentage of genes present in each of the 4 samples was not consistent with about 1.8%-18.7% of genes being detected. Quantitative real-time polymerase chain reaction confirmed that the total RNA purified from each sample was mainly bacterial RNA (Uni 16S) with minimal human mRNA.
CONCLUSION: This study showed that minimal amounts of human RNA were able to be isolated from the saliva of patients with periodontitis as well as controls. Further work is required to enhance the extraction process of human mRNA from saliva if the salivary transcriptome is to be used in determining individual patient susceptibility.