Clinical and radiographic peri‐implant parameters and proinflammatory cytokine levels among cigarette smokers,smokeless tobacco users,and nontobacco users

Background

It is postulated that clinical and radiographic peri‐implant parameters are worse and levels of interleukin (IL)‐1β and matrix metalloproteinase (MMP)‐9 in the peri‐implant sulcular fluid (PISF) are higher in cigarette‐smokers (CS) and smokeless‐tobacco users (STU) compared with nontobacco user (NTU).

Purpose

The present study aimed to compare clinical and radiographic peri‐implant inflammatory parameters and levels of IL‐1β and MMP‐9 levels among CS, STU, and NTU.

Materials and Methods

Forty‐five CS (Group‐1), 42 STU (Group‐2), and 44 NTU (Group‐3) were included. Demographic data was collected using a structured baseline questionnaire. Peri‐implant plaque index (PI), bleeding on probing (BOP), and probing depth (PD) were recorded and crestal bone loss (CBL) were assessed using standardized digital radiographs. PISF volume and levels of IL‐1β and MMP‐9 in PISF were quantified using enzyme‐linked immunosorbent assay. Clinical peri‐implant parameters and PISF IL‐1β and MMP‐9 concentrations were analyzed with Kruskal‐Wallis test. Bonferroni post hoc adjustment test was used for multiple comparisons. P‐value was set at .05.

Results

Peri‐implant PI and PD were significantly worse in group‐1 and group‐2 patients as compared to group‐3 individuals (P < .05). Peri‐implant CBL was also significantly higher in group‐1 and group‐2 compared with group‐3 (P < .05). Peri‐implant BOP was significantly higher in group‐2 and group‐3 as compared to group‐1 individuals (P < .05). The PISF volume (P < .05) collected and levels of IL‐1β and MMP‐9 were statistically significantly elevated among individuals in group‐1 and group‐2 compared with group‐3 (P < .01). There was no significant difference in PI, PD, CBL, and PISF levels of IL‐1β and MMP‐9 among participants in groups 1 and 2.

Conclusion

Clinical and radiographic peri‐implant parameters were compromised among CS and STU as compared to NTU. Increased expression of local proinflammatory cytokines may explain greater susceptibility of CS and STU to peri‐implant breakdown.     

Attenuation of radiation‐ and chemoradiation‐induced mucositis using gamma‐d‐glutamyl‐l‐tryptophan (SCV‐07)

Oral Diseases (2010) 16 , 655–660 Objective: To evaluate the efficacy of a novel immunomodulating peptide (SCV‐07) in attenuating the course of radiation‐induced mucositis in an established animal model of oral mucositis (OM). Material and Methods: In three separate experiments, golden Syrian hamsters received either an acute radiation challenge to the buccal mucosa of eight fractionated doses of 7.5 Gy of radiation over a 2‐week‐period, or a combination of acute radiation and cisplatin. In each experiment, animals were treated with varying doses or schedules of SCV‐07 or placebo. OM was scored in a blinded fashion using digital images obtained during the experimental period. Results: We found that SCV‐07 reduced the severity and duration of both acute and fractionated radiation‐induced OM. Similarly, when radiation and chemotherapy were used to induce OM, treatment with SCV‐07 significantly reduced the duration of ulcerative OM. The therapeutic benefit was dependent on both dose and schedule of administration. Conclusion: Taken together, we found SCV‐07 was able to modify the duration and severity of oral mucositis and was dependent on schedule and dose.     

Interleukin‐1 and interleukin‐8 in nicotine‐ and lipopolysaccharide‐exposed gingival keratinocyte cultures

Johnson GK, Guthmiller JM, Joly S, Organ CC, Dawson DV. Interleukin‐1 and interleukin‐8 in nicotine‐ and lipopolysaccharide‐exposed gingival keratinocyte cultures. J Periodont Res 2010; 45: 583–588. © 2010 John Wiley & Sons A/S Background and Objective: Tobacco use is associated with increased periodontal destruction in both cigarette smokers and smokeless tobacco users. Gingival keratinocytes are the first cells in contact with microbial and tobacco components and play a key role in the innate immune response to these agents. The objective of this study was to evaluate the effect of nicotine and bacterial lipopolysaccharide (LPS) alone and in combination on gingival keratinocyte production of interleukin‐1α (IL‐1α) and interleukin‐8 (IL‐8). Material and Methods: Gingival keratinocyte cultures were established from 10 healthy, non‐tobacco‐using subjects. The cells were stimulated for 24 h with 1 μm or 1 mm nicotine and/or 10 μg/mL Escherichia coli or Porphyromonas gingivalis LPS. Interleukin‐1α and IL‐8 proteins were quantified using ELISAs. Results: Compared with untreated cultures, 1 mm nicotine stimulated production of IL‐1α (p < 0.001); E. coli and P. gingivalis LPS increased IL‐8 production (p = 0.0014 and p = 0.0232, respectively). A combination of nicotine and LPS produced the highest cytokine quantities. Amounts of IL‐1α and IL‐8 following 1 mm nicotine and LPS exposure were significantly greater than in untreated cultures (p < 0.001). Interleukin‐8 was also responsive to 0.1 μm nicotine combined with E. coli or P. gingivalis LPS compared with control cultures (p < 0.0001 and p = 0.0029, respectively). Both cytokines tended to be elevated following the combined treatment relative to nicotine or LPS treatment alone. Conclusion: These results demonstrate that nicotine and LPS differentially regulate IL‐1 and IL‐8 production by gingival keratinocytes. Combined treatment tended to elevate cytokine production further, which may have implications for the progression of periodontitis in tobacco users.     

Cell‐to‐cell interactions

The narrow anatomic periodontal space between the root surface and the alveolar bone is relatively poor in cells. However, a broad range of noxious stimuli, most frequently root canal infection, will result in the accumulation of a large number of inflammatory cells in the periapical region of the affected tooth/root. The encounter between invading microorganisms and host cells as well as the interactions of resident and immigrating cells will determine the course of the inflammatory events that may take place. This review attempts to summarize current knowledge on how cellular interactions may contribute to dynamic equilibrium between protective, self‐maintaining, propagating, destructive and downregulating events in apical periodontitis.     

Insulin‐like growth factor‐binding protein‐2 and ‐3 in gingival crevicular fluid

Takenouchi Y, Ohshima M, Yamaguchi Y, Nishida T, Senda N, Idesawa M, Otsuka K, Ito K. Insulin‐like growth factor‐binding protein‐2 and ‐3 in gingival crevicular fluid. J Periodont Res 2010; 45: 803–808. © 2010 John Wiley & Sons A/S Background and Objective: Insulin‐like growth factor‐binding proteins (IGFBPs) are crucial regulators of insulin‐like growth factor (IGF). They enhance or inhibit IGF functions, but also exhibit IGF‐independent effects. In a previous study, we detected, qualitatively, IGFBP‐2 and ‐3 in gingival crevicular fluid using a cytokine antibody array. Here we extended these results using an ELISA to determine the concentrations of IGFBP‐2 and ‐3 in gingival crevicular fluid. In addition, we explored whether the expression of IGFBP‐2 and IGFBP‐3 correlates with periodontal disease severity. Material and Methods: Gingival crevicular fluid samples from 92 sites of 12 patients affected with periodontal disease and from 100 sites of 19 healthy volunteers, were collected, divided into two groups and analyzed by ELISA for IGFBP‐2 and ‐3 expression. The potential correlation among probing depth, gingival index and the concentrations of IGFBP‐2 and ‐3 was analyzed. Results: Positive correlations were observed between the concentration of IGFBP‐2 and probing depth and gingival index, but not for IGFBP‐3. The IGFBP‐2 concentrations at bleeding on probing‐positive sites and at sites with a probing depth of ≥ 4 mm were higher than at bleeding on probing‐negative sites and at sites with a probing depth of ≤ 3 mm. Conclusion: These results indicate that IGFBP‐2 is a potential novel marker for periodontal disease progression. As IGFBP‐2 modulates bone metabolism and cell migration, IGFBP‐2 in the gingival crevicular fluid may reflect periodontal disease activity.