A Novel Connective Tissue Graft Harvesting Technique: The Ring Method.

The aim of these case reports was to introduce a simplified novel connective tissue graft (CTG) harvesting technique, the ring method, which could be used in the maxillary tuberosity area in particular. A special CTG harvesting punch was fabricated to obtain a ring-shaped CTG that had a uniform thickness. The ring graft was then used for peri-implant soft tissue augmentation with successful clinical outcomes. The ring method is a technically insensitive and minimally invasive surgical procedure that provides a certain amount of CTG for various periodontal plastic surgical interventions.

A novel soft tissue thickness measuring method using cone beam computed tomography.

OBJECTIVE: The aim of this study was to introduce a novel soft tissue thickness measurement method using cone beam computed tomography (CBCT) and to compare the new method with ultrasonic device applications and transgingival probing measurements. METHODS: Twenty-five participants (12 female, 13 male, age range, 25-51 years) were included the study. Soft tissue thickness in lateral incisor, canine, premolar, and molar regions were measured using transgingival probing (group T), ultrasonic device (group U), and CBCT scan measurements (group C). Differences and correlations between groups and agreement between measurement methods were evaluated. RESULTS: Soft tissue thickness was significantly lower in group U in premolar region, but was significantly higher in molar region compared with group C and group T (P < .05). There were significant positive correlations in lateral incisor and canine region, between group U and group C, in premolar region between group T and group C, and in molar region between group U and group C, and between group C and group T (P < .05). The highest agreement between measurement methods was evident between group T and group C. CONCLUSION: Soft tissue thickness values in maxilla may differ depending on the measurement method and location of the measurement. Ultrasonic device, transgingival probing, and CBCT measures may not necessarily correlate in all locations. The high agreement between CBCT measurements and transgingival probing may suggest the newly introduced method as a promising technique for soft tissue thickness evaluation. CLINICAL SIGNIFICANCE: This study evaluated the relation between different soft tissue thickness measurement methods and demonstrated a novel method which can be used in any part of the mouth. The outcome also suggested that the measurement method and the location might affect the soft tissue thickness value obtained, and therefore might be important in clinical decision making.

Intraoral versus extraoral cementation of implant-supported single crowns: Clinical, biomarker, and microbiological comparisons.

OBJECTIVES: Implant supported single metal-ceramic crowns cemented either extraorally or intraorally were comparatively evaluated by clinical, radiologic, biomarker, and microbiological parameters. MATERIALS AND METHODS: Twelve patients with bilateral single tooth gap in the maxillary posterior region received two locking-taper implants; 4.5 mm width, 8 mm length. Selection of intraoral (IOC) or extraoral cementation (EOC) using screwless titanium abutments was done randomly. Peri-implant crevicular fluid (PICF), gingival crevicular fluid (GCF) samples were collected from the implants, adjacent teeth, and bleeding on probing, soft tissue thickness, keratinized tissue width were recorded before starting the prosthetic procedures (baseline) and 3, 6 months after implant loading. Crestal bone loss was measured on radiographs taken immediately and 6 months after cementation. Cytokine levels, amounts of bacteria were determined in PICF/GCF samples. Data were tested by appropriate statistical analyses. RESULTS: Clinical findings were similar in the crowns cemented extraorally or intraorally at all times (P < .05). PICF and GCF data were similar. At 3 month, interleukin-17E and osteoprotegerin levels were lower in the intraorally cemented crowns. CONCLUSION: Extraorally and intraorally cemented crowns exhibited similar crestal bone loss after loading. Higher amount of osteoprotegerin at 3 month at the EOC than the IOC sites might bode well for good osseointegration.

Do salivary and serum collagenases have a role in an association between obstructive sleep apnea syndrome and periodontal disease? A preliminary case-control study.

OBJECTIVES: Despite increasing evidence for an association of obstructive sleep apnea syndrome (OSAS) and periodontal disease, the pathophysiological linking mechanisms remain unclear. This study aims to evaluate the salivary and serum matrix metalloproteinase-2, -8, -9 (MMP-2, -8, -9), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), myeloperoxidase (MPO), neutrophil elastase (NE), neutrophil gelatinase-associated lipocalin (NGAL), as well as degree of activation of MMP-2, -9 of patients with and without OSAS. DESIGN: A total of 50 individuals were included in the study. There were 13, 17 and 20 individuals, respectively in the control (non-OSAS) group, mild-to-moderate OSAS and severe OSAS groups. Saliva, serum samples and clinical periodontal parameters were collected. Biofluid samples were analysed by immunofluorometric assay (IFMA), enzyme-linked immunosorbent assay (ELISA), western immunoblotting and gelatine zymography. Statistical analyses were performed using D'Agostino-Pearson omnibus normality test, Kruskal-Wallis test and Spearman rho rank correlation analysis. RESULTS: There were no statistically significant differences in clinical periodontal parameters between the study groups. Salivary NE and proMMP-2 levels were significantly lower in the OSAS groups than the control group (p<0.05). Serum proMMP-9 concentration and the degree of MMP-9 activation in saliva were significantly lower in the severe OSAS group than the control group (p<0.05). There were significant correlations between salivary and serum proMMP-9 and -2 concentrations (p<0.05). Serum proMMP-2, NE and salivary proMMP-9 and -2 negatively correlated with indicators of OSAS severity (p<0.05). CONCLUSIONS: The present findings do not support a pathophysiological link between the severity of OSAS and clinical periodontal status via neutrophil enzymes or MMPs.

Serum and salivary matrix metalloproteinases, neutrophil elastase, myeloperoxidase in patients with chronic or aggressive periodontitis.

Salivary, serum matrix metalloproteinase-8 (MMP-8), tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), neutrophil elastase (NE), and myeloperoxidase (MPO) levels were investigated in generalized chronic periodontitis (GCP), generalized aggressive periodontitis (GAgP), and healthy groups. Whole-mouth clinical periodontal measurements were recorded. Salivary, serum concentrations of MMP-8, MPO, TIMP-1, and NE were determined by immunofluorometric assay or ELISA in 18 patients with GCP, 23 patients with GAgP, 18 individuals with healthy periodontium. Patients in the GAgP group were younger than the other groups (p<0.05). The study groups were similar in gender, smoking status. Plaque index was higher in GCP than GAgP group (p<0.05). Biochemical data were similar in periodontitis groups. Salivary, serum MPO, and salivary NE concentrations were higher; TIMP-1 concentrations were lower in the periodontitis groups than the controls (p<0.05). The present data support a close relationship between salivary, serum protease content and clinical periodontal parameters in patients with generalized periodontitis.

Salivary cytokines and the association between obstructive sleep apnea syndrome and periodontal disease.

BACKGROUND: A higher prevalence of periodontal disease has been reported in patients with obstructive sleep apnea syndrome (OSAS), and these two chronic conditions may be linked via inflammatory pathways. The aim of the present study is to evaluate the salivary interleukin (IL)-1ß, IL-6, IL-21, IL-33, and pentraxin-3 (PTX3) concentrations in patients with and without OSAS. METHODS: A total of 52 patients were included in the study. Thirteen individuals were in the control (non-OSAS) group, 17 were in the mild/moderate OSAS group, and 22 were in the severe OSAS group. Clinical periodontal measurements were recorded, and saliva samples were obtained before initiation of periodontal intervention. Enzyme-linked immunosorbent assay was used to determine salivary cytokine concentrations. Data were statistically analyzed using D'Agostino-Pearson omnibus normality, Spearman ρ rank, Kruskal-Wallis, and Dunn tests. RESULTS: Salivary IL-6 and IL-33 concentrations were similar in the two OSAS groups (P >0.05), which were statistically higher than the control group (P <0.05). IL-1ß, IL-21, and PTX3 concentrations were similar in the study groups. The only significant correlation between clinical periodontal parameters and salivary cytokines was found between clinical attachment level (CAL) and IL-21 (P = 0.02). Highly significant correlations were found between probing depth, CAL measures, and indicators of OSAS severity (P <0.01). CONCLUSIONS: The present findings suggest that OSAS may have an increasing effect on salivary IL-6 and IL-33 concentrations regardless of OSAS severity. Additional investigation is required to elucidate a potential bidirectional relationship between OSAS and periodontal disease.

Saliva and serum levels of B-cell activating factors and tumor necrosis factor-α in patients with periodontitis.

BACKGROUND: B-lymphocytes play a central and critical role in the adaptive immune response against invading pathogens. This study evaluates saliva and serum levels of APRIL (a proliferation-inducing ligand), B-cell activating factor (BAFF), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-10 in patients with chronic periodontitis (CP) or aggressive periodontitis (AgP) and periodontally healthy individuals. METHODS: Twenty-five patients with AgP, 20 patients with CP, and 20 periodontally healthy individuals were included. Smoking status was recorded, and all individuals were divided into non-smokers and smokers. Saliva and serum samples were collected before clinical periodontal measurements. APRIL, BAFF, TNF-α, IL-6, and IL-10 levels in serum and saliva samples were determined by enzyme-linked immunosorbent assay. Statistical analysis was performed using multivariate analysis of variance and bivariate correlation. RESULTS: Serum and saliva levels of TNF-α, APRIL, BAFF, IL-6, and IL-10 were similar in CP and AgP groups. Serum levels of TNF-α, APRIL, and BAFF and saliva levels of BAFF were significantly higher in periodontitis groups than healthy controls (P <0.05). Non-smokers with CP or AgP had lower levels of saliva TNF-α and APRIL and serum APRIL and IL-6 than smokers with CP or AgP (P <0.05). Saliva APRIL and serum TNF-α and IL-6 levels were significantly higher in healthy smokers than healthy non-smokers (P <0.05). Clinical periodontal parameters correlated positively with TNF-family cytokines and negatively with IL-10 (P <0.05). CONCLUSIONS: Within the limits of this study, it may be suggested that elevated salivary and serum TNF-α, APRIL, and BAFF in patients with periodontitis may contribute to the dominance of B cells in periodontitis lesions. Moreover, higher levels in healthy smokers than non-smoking counterparts may play a role in detrimental effects of smoking on periodontal tissues.

Saliva and serum levels of pentraxin-3 and interleukin-1ß in generalized aggressive or chronic periodontitis.

BACKGROUND: Pentraxin-3 (PTX3) is a multifactorial protein involved in immunity and inflammation, which is rapidly produced and released by several cell types in response to inflammatory signals. The aim of the present study is to evaluate saliva, serum levels of PTX3, interleukin (IL)-1ß in patients with generalized chronic periodontitis (CP) or aggressive periodontitis (AgP), and periodontally healthy individuals. METHODS: A total of 94 participants (25 patients with AgP, 25 patients with CP, and 44 periodontally healthy individuals matched with AgP and CP groups) were recruited. Saliva and serum samples were collected. Clinical periodontal measurements were recorded. PTX3, IL-1ß levels in serum, and saliva samples were determined by enzyme-linked immunosorbent assay. Data were tested statistically using Kruskal-Wallis, Mann-Whitney U, and Spearman ρ rank test. RESULTS: Serum and saliva data were similar in CP and AgP groups. Saliva levels of IL-1ß were significantly higher in the AgP and CP groups than controls (P <0.05). Salivary PTX3 levels were similar in the CP and control groups. Significantly higher salivary concentrations of PTX3 were detected in the AgP group than the control group (P <0.05). Saliva PTX3 levels correlated with plaque index and bleeding on probing in the CP group (P <0.05). Serum and saliva PTX3 levels correlated with those of IL-1ß in the AgP group (P <0.05). CONCLUSIONS: It may be suggested that PTX3 is related with periodontal tissue inflammation. Its salivary concentrations may have a diagnostic potential. Additional intervention and follow-up studies coupling PTX3 concentrations with microbiologic analysis would better clarify its role in periodontal diseases.

Altered antigenic profiling and infectivity of Porphyromonas gingivalis in smokers and non-smokers with periodontitis.

BACKGROUND: Cigarette smokers are more susceptible to periodontal diseases and are more likely to be infected with Porphyromonas gingivalis than non-smokers. Furthermore, smoking is known to alter the expression of P. gingivalis surface components and compromise immunoglobulin (Ig)G generation. The aim of this study is to evaluate whether the overall IgG response to P. gingivalis is suppressed in smokers in vivo and whether previously established in vitro tobacco-induced phenotypic P. gingivalis changes would be reflected in vivo. METHODS: The authors examined the humoral response to several P. gingivalis strains as well as specific tobacco-regulated outer membrane proteins (FimA and RagB) by enzyme-linked immunosorbent assay in biochemically validated (salivary cotinine) smokers and non-smokers with chronic periodontitis (CP: n = 13) or aggressive periodontitis (AgP: n = 20). The local and systemic presence of P. gingivalis DNA was also monitored by polymerase chain reaction. RESULTS: Smoking was associated with decreased total IgG responses against clinical (10512, 5607, and 10208C; all P <0.05) but not laboratory (ATCC 33277, W83) P. gingivalis strains. Smoking did not influence IgG produced against specific cell-surface proteins, although a non-significant pattern toward increased total FimA-specific IgG in patients with CP, but not AgP, was observed. Seropositive smokers were more likely to be infected orally and systemically with P. gingivalis (P <0.001), as determined by 16S RNA analysis. CONCLUSION: Smoking alters the humoral response against P. gingivalis and may increase P. gingivalis infectivity, strengthening the evidence that mechanisms of periodontal disease progression in smokers may differ from those of non-smokers with the same disease classification.

Low-level laser irradiation affects the release of basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I), and receptor of IGF-I (IGFBP3) from osteoblasts.

OBJECTIVE: It was the aim of the present study to evaluate whether the laser irradiation of osteoblasts could enhance the release of growth factors including basic fibroblast growth factor (bFGF), insulin-like growth factor-I (IGF-I), and receptor of IGF-I (IGFBP3). BACKGROUND DATA: Low-level laser therapy (LLLT) has been shown to have biostimulatory effects on various cell types by enhancing production of some cytokines and growth factors. MATERIALS AND METHODS: Human mesenchymal stem cells (MSCs) were seeded in osteogenic medium and differentiated into osteoblasts. Three groups were formed: in the first group (single dose group), osteoblasts were irradiated with laser (685 nm, 25 mW, 14.3 mW/cm(2), 140 sec, 2 J/cm(2)) for one time; and in the second group, energy at the same dose was applied for 2 consecutive days (double dose group). The third group was not irradiated with laser and served as the control group. Proliferation, viability, bFGF, IGF-I, and IGFBP3 levels were compared between groups. RESULTS: Both of the irradiated groups revealed higher proliferation, viability, bFGF, IGF-I, and IGFBP3 expressions than did the nonirradiated control group. There was increase in bFGF and IGF-I expressions and decrease in IGFBP3 in the double dose group compared to single dose group. CONCLUSIONS: The results of the present study indicate that LLLT increases the proliferation of osteoblast cells and stimulates the release of bFGF, IGF-I, and IGFBP3 from these cells. The biostimulatory effect of LLLT may be related to the enhanced production of the growth factors.

Therapeutic efficacy of vasoactive intestinal peptide in escherichia coli lipopolysaccharide-induced experimental periodontitis in rats.

BACKGROUND: The aim of the present study was to evaluate the therapeutic efficacy of vasoactive intestinal peptide (VIP), an immunoregulatory molecule, in experimental periodontitis. METHODS: Sixty-three male Sprague-Dawley rats were divided into five groups: control; lipopolysaccharide (LPS); LPS + 0.1 nmol VIP; LPS + 1 nmol VIP; and LPS + 10 nmol VIP. Saline was injected into the gingiva of control rats on days 1, 3, and 5, whereas the other groups received injections of Escherichia coli LPS. VIP groups received intraperitoneal injections of relevant dosages on days 2, 4, 6, 8, and 10. The control and LPS groups were given saline instead of VIP in the same manner. On day 11, serum samples were obtained, and rats were sacrificed. Alveolar bone loss; serum levels of tumor necrosis factor-alpha, interleukin (IL)-1beta, -10, and -18, soluble receptor activator of nuclear factor-kappa B ligand (sRANKL), and osteoprotegerin (OPG); and the immune expression of RANKL and OPG were evaluated. RESULTS: The application of VIP caused a dose-dependent decline in alveolar bone loss compared to the LPS group, but the differences were not significant (P >0.05). A reduction in the histologic findings of inflammation was observed in all VIP groups. The 1- and 10-nmol VIP groups showed significantly lower serum sRANKL and OPG levels compared to the LPS group (P <0.05). The number of positively stained vessels for endothelial OPG was greater in the 1-nmol VIP group than in the LPS group (P <0.05). CONCLUSION: When periodontitis was induced by E. coli LPS, VIP downregulated the inflammatory response and inhibited alveolar bone loss, possibly by differentially regulating the tissue levels of RANKL and OPG.