Increased interleukin‐18 in gingival crevicular fluid from periodontitis patients

Introduction: This study aimed to measure the levels of interleukin‐18 (IL‐18) in inflamed shallow sites and inflamed deep sites in patients with periodontitis and to compare the data with results from inflamed shallow sites in patients with gingivitis. A secondary aim was to examine the composition of the subgingival microbiota in the sampled sites. Methods: Gingival crevicular fluid was collected from five gingivitis sites and five periodontitis sites from 18 patients with chronic periodontitis, and from five gingivitis sites from 15 patients with gingivitis. Samples from each site category were pooled and IL‐18 levels were measured using an enzyme‐linked immunosorbent assay. The subgingival microbiota was analyzed by checkerboard DNA–DNA hybridization. Results: All clinical parameters and gingival crevicular fluid volumes were higher in periodontitis sites compared with gingivitis sites from patients with periodontitis and gingivitis. The total amount of IL‐18 was higher in periodontitis sites than gingivitis sites in both periodontitis (P = 0.018) and gingivitis (P = 0.002) patients and was higher in gingivitis sites from periodontitis patients than in those from gingivitis patients (P = 0.015). There were higher levels of Tannerella forsythia, Porphyromonas gingivalis, and Treponema denticola (red complex species) in periodontitis sites compared with gingivitis sites in both the periodontitis and gingivitis patients (P < 0.001). Conclusion: Levels of IL‐18 were higher in patients with chronic periodontitis compared with patients with gingivitis, even at sites with similar pocket depths. The presence of similar levels of red complex species in gingivitis sites from periodontitis patients and from gingivitis patients suggested that the higher levels of IL‐18 were not associated with a different microbial challenge.     

Prevalence of periodontitis and DMFT index in patients with Crohn's disease and ulcerative colitis

Aim: To compare the prevalence of periodontal disease and the decayed, missing and filled teeth (DMFT) index in patients with Crohn's disease (CD) and ulcerative colitis (UC) with those without these diseases. Material and Methods: Ninety‐nine CD (39.0 SD±12.9 years), 80 UC (43.3 SD±13.2) and 74 healthy controls (40.3 SD±12.9) were compared for DMFT index and presence of periodontitis. Probing pocket depth (PPD), clinical attachment loss (CAL), bleeding on probing (BOP), plaque and DMFT index were measured on all subjects. The presence of periodontitis was defined as having CAL 3 mm in at least four sites in different teeth. Results: Significantly more patients with UC (90.0%; p<0.001) and CD (81.8%; p=0.03) had periodontitis than controls (67.6%). Among smokers, UC patients had significantly more periodontitis. CD had a greater mean DMFT score (18.7 versus 13.9; p=0.031) compared with controls and UC had greater median PPD (2.2 versus 1.7 mm; p<0.0001) than controls. Among non‐smokers, CD (2.4 mm; p<0.0001) and UC showed deeper pockets (2.3 mm; p<0.0001) compared with controls (1.5 mm). UC had a greater mean DMFT score (15.3 versus 12.1; p=0.037) compared with controls. Conclusions: CD and UC patients had higher DMFT and prevalence of periodontitis than controls, but smoking was an effect modifier.     

Periodontal conditions in patients with juvenile idiopathic arthritis

OBJECTIVE: Our aim was to compare the periodontal conditions in a group of juvenile idiopathic arthritis (JIA) patients with those in a control group of healthy subjects (CTR). MATERIAL AND METHODS: Thirty-two patients with JIA and 24 controls were selected. The measurements used to diagnose periodontal disease included plaque and bleeding scores, probing depths (PDs) and clinical attachment loss (CAL). Laboratory indicators of JIA activity included the erythrocyte sedimentation rate (ESR) and capsule-reactive protein (CRP). The Mann-Whitney test was used to evaluate the data (alpha = 0.05). RESULTS: The mean ages were 15.9 (+/- 2.7) years and 14.7 (+/- 2.3) years for groups JIA and CTR, respectively. The median ESR was 42 mm/h 13 mm/h in the CTR group (p = 0.032) and the median CRP was 1.9 and 0.4 mg/l, respectively (p = 0.001). The prevalence of patients with a proximal attachment loss of 2mm or more in the JIA group was 25% and in controls it was 4.2%. The mean percentages of visible plaque and marginal bleeding were similar in the JIA (54 +/- 22 and 30 +/- 16, respectively) and CTR groups (44 +/- 18 and 29 +/- 11, respectively). The mean percentages of sites with PD > or = 4 mm were significantly higher in the JIA group (3 +/- 4.7) than in the CTR group (0.4 +/- 1.7) (p = 0.012). The mean percentages of sites with proximal CAL > or = 2 mm were 0.7 (+/- 1.4) in the JIA group and 0.001 (+/- 0.2) in the CTR group (p = 0.022). CONCLUSION: Adolescents with JIA present more periodontal attachment loss than healthy controls, in spite of similar plaque and marginal bleeding levels.     

Factors Associated with Treatment Compliance in a Population of Juvenile Sexual Offenders

Structural equation modeling was utilized to assess predictors of outcomes in a sample of 204 juvenile male sexual offenders participating in community-based treatment programming. Lower levels of client denial at intake predicted successful program compliance. Higher levels of denial were found in nonadjudicated youths. Although program attrition was high (50% in the first year), relatively few youths were expelled for sexual (4.9%) or nonsexual delinquency (6.6%) over a 12- to 24-month period. Program failure during years 1 and 2 was attributable largely to expulsion for failure to comply with attendance requirements and/or therapeutic directives. Youths failing to comply were found to have higher overall levels of measured sexual maladjustment and may be at greater long-term risk for sexual recidivism. Implications of the findings for clinical risk assessment, and directions for future research, are discussed.     

siRNA knockdown of mitochondrial thymidine kinase 2 (TK2) sensitizes human tumor cells to gemcitabine

Nucleoside metabolism enzymes are determinants of chemotherapeutic drug activity. The nucleoside salvage enzyme deoxycytidine kinase (dCK) activates gemcitabine (2′, 2′-difluoro-2′-deoxycytidine) and is negatively regulated by deoxycytidine triphosphate (dCTP). Reduction of dCTP in tumor cells could, therefore, enhance gemcitabine activity. Mitochondrial thymidine kinase 2 (TK2) phosphorylates deoxycytidine to generate dCTP. We hypothesized that: (1) TK2 modulates human tumor cell sensitivity to gemcitabine, and (2) antisense knockdown of TK2 would decrease dCTP and increase dCK activity and gemcitabine activation. siRNA downregulation of TK2 sensitized MCF7 and HeLa cells (high and moderate TK2) but not A549 cells (low TK2) to gemcitabine. Combined treatment with TK2 siRNA and gemcitabine increased dCK. We also hypothesized that TK2 siRNA-induced drug sensitization results in mitochondrial damage that enhances gemcitabine effectiveness. TK2 siRNA and gemcitabine decreased mitochondrial redox status, DNA content, and activity. This is the first demonstration of a direct role for TK2 in gemcitabine resistance, or any independent role in cancer drug resistance, and further distinguishes TK2 function from that of other dTMP-producing enzymes [cytosolic TK1 and thymidylate synthase (TS)]. siRNA knockdown of TK1 and/or TS did not sensitize cancer cells to gemcitabine indicating that, among the 3 enzymes, only TK2 is a candidate therapeutic target for combination with gemcitabine.