Mural cell composition and functional analysis in the healing process of human gingiva from periodontal intrabony defects.

OBJECTIVE: To evaluate the composition and function of mural cell populations in human gingival tissues DESIGN: A cross-sectional study was conducted on seven periodontitis (stage Ⅲ) patients. Gingival tissues were collected two months after scaling and root planing and divided into 3 groups: 1, h_h group (horizontal bone resorption, residual pocket depth ≤3 mm); 2, v_h group (vertical bone resorption >4 mm, residual pocket depth ≤3 mm); 3, v_i group (vertical bone resorption >4 mm, residual pocket depth ≥6 mm). Single-cell RNA sequencing (10X genomics) and subsequent bioinformatics analysis were performed. Protein expression of selected genes was confirmed by histological staining. RESULTS: Two mural cell clusters, RGS5+THY1+ and ACTA2+MYH11+ subpopulations, were identified and confirmed by histological staining and cross-validation with three different single-cell RNA sequencing datasets in the GEO database. RGS5+THY1+ cluster in perivascular areas possessed cellular protrusions and exhibited immunomodulatory and synthetic phenotypes. In contrast, the ACTA2+MYH11+ cluster strictly distributed around vessel walls was characterized by a contractile phenotype. Mural cells closely interacted with endothelial cells through PDGF and NOTCH3 signaling. Mural cell loss was detected in the v_i group and in hopeless periodontal teeth, which might be caused by tumor necrosis factor-alpha induced apoptosis. CONCLUSIONS: Gingival mural cells can be classified into two distinct clusters according to their gene signatures and cell morphology. The loss of mural cells may indicate periodontitis progression.

Clinical attachment loss and molecular profile of inflamed sites before treatment.

OBJECTIVE: To monitor early periodontal disease progression and to investigate clinical and molecular profile of inflamed sites by means of crevicular fluid and gingival biopsy analysis. METHODOLOGY: Eighty-one samples of twenty-seven periodontitis subjects and periodontally healthy individuals were collected for the study. Measurements of clinical parameters were recorded at day -15, baseline and 2 months after basic periodontal treatment aiming at monitoring early variations ofthe clinical attachment level. Saliva, crevicular fluid and gingival biopsies were harvested from clinically inflamed and non-inflamed sites from periodontal patients and from control sites of healthy patients for the assessment of IL-10, MMP-8, VEGF, RANKL, OPG and TGF-ß1 protein and gene expression levels. RESULTS: Baseline IL-10 protein levels from inflamed sites were higher in comparison to both non-inflamed and control sites (p<0.05). Higher expression of mRNA for IL-10, RANK-L, OPG, e TGF-ß1 were also observed in inflamed sites at day -15 prior treatment (p<0.05). After the periodontal treatment and the resolution of inflammation, seventeen percent of evaluated sites still showed clinically detectable attachment loss without significant differences in the molecular profile. CONCLUSIONS: Clinical attachment loss is a negative event that may occur even after successful basic periodontal therapy, but it is small and limited to a small percentage of sites. Elevated inflammation markers of inflamed sites from disease patients reduced to the mean levels of those observed in healthy subjects after successful basic periodontal therapy. Significantly elevated both gene and protein levels of IL-10 in inflamed sites prior treatment confirms its modulatory role in the disease status.

The effect of nonsurgical periodontal therapy on hepcidin and on inflammatory and iron marker levels.

Serum hepcidin levels may increase in response to infection and inflammation. The present study investigated the effect of nonsurgical periodontal therapy (NSPT) on levels of serum hepcidin, inflammatory markers, and iron markers. An interventional study was conducted on 67 patients (age 30-65 years) without other diseases, except for chronic periodontitis (CP). Patients were allocated to either CP or control groups. The CP group received supragingival and subgingival scaling and root planing procedures, whereas the control group received supragingival scaling. Probing depth (PD), bleeding on probing, clinical attachment level (CAL), visible plaque index (VPI), serum hepcidin and interleukin-6 (IL-6) levels, high-sensitivity C-reactive protein (hs-CRP), hematological markers, and iron markers were measured at baseline and at 90 days after NSPT. The CP group had statistically significant lower mean values for mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) (p ≤ 0.05). The control group had statistically significant reductions in hemoglobin, hematocrit, MCV, and MCH (p ≤ 0.05). Serum hepcidin, IL-6, and erythrocyte sedimentation rate (ESR) levels were significantly decreased in both groups after NSPT. Periodontal markers were more markedly reduced in the CP group compared with the control group (p ≤ 0.05). These findings suggest that NSPT may reduce the serum levels of IL-6, hepcidin, and periodontal parameters.

Associations of chairside salivary aMMP-8 findings with periodontal parameters, potentially periodontal pathogenic bacteria and selected blood parameters in systemically healthy adults.

The aim of this cross-sectional study was to investigate associations between salivary active matrix-metalloproteinase 8 (aMMP-8) and periodontitis severity, potentially periodontal pathogenic bacteria as well as blood parameters in generally healthy participants. Therefore, 188 participants with a mean age of 48.9 ±â€¯8 years were examined. The periodontitis severity was assessed based on periodontal probing depth and clinical attachment loss. Both, aMMP-8 and microbiological analysis were performed using a validated, commercially available test system. Blood values were utilized from regular differential blood count. The aMMP-8 findings were associated with the periodontitis severity (P < 0.01), as well as with the prevalence of Porphyromonas gingivalis, Tannerella forsythia, Prevotella intermedia, Parvimonas micra, Camphylobacter rectus and Eubacterium nodatum (Pi < 0.05). No associations between aMMP-8 and the examined blood parameters were found (Pi > 0.05). In conclusion, salivary aMMP-8 findings seem to reflect periodontal disease severity as a result of an immunoreaction, especially against bacteria with high periodontal pathogenic potential.

High salivary levels of JP2 genotype of Aggregatibacter actinomycetemcomitans is associated with clinical attachment loss in Moroccan adolescents.

It has previously been shown that the presence of Aggregatibacter actinomycetemcomitans in subgingival plaque is significantly associated with increased risk for clinical attachment loss. The highly leukotoxic JP2 genotype of this bacterium is frequently detected in adolescents with aggressive forms of periodontitis. The aims of the study were to quantify the levels of JP2 and non-JP2 genotypes of A. actinomycetemcomitans in saliva of Moroccan adolescents with the JP2 genotype earlier detected in the subgingival plaque. The salivary concentrations of inflammatory proteins were quantified and linked to the clinical parameters and microbial findings. Finally, a mouth rinse with leukotoxin-neutralizing effect was administrated and its effect on the levels the biomarkers and A. actinomycetemcomitans examined. The study population consisted of 22 adolescents that previously were found to be positive for the JP2 genotype in subgingival plaque. Periodontal registration and sampling of stimulated saliva was performed at baseline. A mouth rinse (active/placebo) was administrated, and saliva sampling repeated after 2 and 4 weeks rinse. The salivary levels of JP2 and non-JP2 were analyzed by quantitative PCR and inflammatory proteins by ELISA. Both the JP2 and the non-JP2 genotype were detected in all individuals with significantly higher levels of the non-JP2. Enhanced levels of the JP2 genotype of A. actinomycetemcomitans was significantly correlated to the presence of attachment loss (≥3 mm). Salivary concentrations of inflammatory biomarkers did not correlate to periodontal condition or levels of A. actinomycetemcomitans. The use of active or placebo leukotoxin-neutralizing mouth rinse did not significantly interfered with the levels of these biomarkers. Saliva is an excellent source for detection of A. actinomycetemcomitans on individual basis, and high levels of the JP2 genotype were significantly associated with the presence of clinical attachment loss.

Association of initial mucogingival status with clinical outcome of non-surgical periodontal therapy: A retrospective analysis of 204 patients.

BACKGROUND/PURPOSE: This study was conducted to evaluate the influence of mucogingival parameters, including keratinized mucosa (KM) and attached gingiva (AG), on the outcome of non-surgical periodontal therapy (NSPT). METHODS: A total of 204 non-smoking patients with generalized chronic periodontitis who received NSPT between 2012 and 2014 were included. The Mantel-Haenszel chi-square test was used to assess the associations between initial mucogingival parameters and initial clinical parameters on the buccal aspect, and the associations between initial mucogingival parameters and outcome clinical parameters on the buccal aspect of the sites with severe periodontal destruction. The generalized liner model was used to evaluate the contribution of initial clinical parameters to the outcome of NSPT. RESULTS: KM ≥ 3 mm was associated with greater probing pocket depth (PD), less gingival recession (REC), and less clinical attachment level (CAL), and AG < 1 mm was associated with greater PD, REC, and CAL before NSPT. At the sites with severe periodontal destruction, KM ≥ 3 mm was associated with greater PD reduction (0.25 ± 0.08 mm) and CAL gain (0.25 ± 0.09 mm), and AG < 1 mm was associated with greater CAL gain (0.15 ± 0.08 mm) after NSPT. Initial PD ≥ 7 mm and non-molar teeth showed greater contribution to the outcome of NSPT. CONCLUSION: Less AG (<1 mm) was associated with greater periodontal destruction at baseline. At the sites with severe periodontal destruction, greater KM (≥3 mm) and less AG (<1 mm) resulted in better outcomes of NSPT.

Clinical Characteristics of Abutment Teeth with Gingival Discoloration.

PURPOSE: The grey-bluish discoloration of gingiva (known as "amalgam tattoo") does not appear only in the presence of amalgam restorations. It may also be seen in cases of teeth restored with cast dowels and porcelain-fused-to-metal (PFM) restorations. The aim of this article was to determine the clinical characteristics of abutment teeth with gingival discoloration. MATERIALS AND METHODS: This research was conducted on 25 patients referred for cast dowel and PFM restorations. These restorations were manufactured from Ni-Cr alloys. Ninety days after cementing the fixed prosthodontic restorations, the abutment teeth (n = 61) were divided into a group with gingival discoloration (GD) (n = 25) and without gingival discoloration (NGD) (n = 36). The control group (CG) comprised the contralateral teeth (n = 61). Plaque index, gingival index, clinical attachment level, and probing depth were assessed before fabrication and also 90 days after cementation of the PFM restorations. RESULTS: The gingival index, clinical attachment level, and probing depths of the abutment teeth that had GD were statistically higher before restoration, in comparison with the abutment teeth in the NGD and control groups. Ninety days after cementation, the abutment teeth with GD had significantly lower gingival indexes and probing depths, compared to the abutment teeth in the NGD group. Both abutment teeth groups (GD and NGD) had significantly higher values of clinical attachment levels when compared to the control group. There were no statistically significant differences in plaque index values between the study groups. CONCLUSIONS: The results of this study indicated that impairment of periodontal status of abutment teeth seemed to be related to the presence of gingival discolorations. Therefore, fabrication of fixed prosthodontic restorations requires careful planning and abutment teeth preparation to minimize the occurrence of gingival discolorations. CLINICAL RELEVANCE: With careful preparation of abutment teeth for cast dowels and crown restorations it may be possible to decrease the frequency of gingival discolorations adjacent to abutment teeth.

Clinical attachment loss and molecular profile of inflamed sites before treatment

Abstract Objective: To monitor early periodontal disease progression and to investigate clinical and molecular profile of inflamed sites by means of crevicular fluid and gingival biopsy analysis. Methodology: Eighty-one samples of twenty-seven periodontitis subjects and periodontally healthy individuals were collected for the study. Measurements of clinical parameters were recorded at day −15, baseline and 2 months after basic periodontal treatment aiming at monitoring early variations ofthe clinical attachment level. Saliva, crevicular fluid and gingival biopsies were harvested from clinically inflamed and non-inflamed sites from periodontal patients and from control sites of healthy patients for the assessment of IL-10, MMP-8, VEGF, RANKL, OPG and TGF-β1 protein and gene expression levels. Results: Baseline IL-10 protein levels from inflamed sites were higher in comparison to both non-inflamed and control sites (p<0.05). Higher expression of mRNA for IL-10, RANK-L, OPG, e TGF-β1 were also observed in inflamed sites at day −15 prior treatment (p<0.05). After the periodontal treatment and the resolution of inflammation, seventeen percent of evaluated sites still showed clinically detectable attachment loss without significant differences in the molecular profile. Conclusions: Clinical attachment loss is a negative event that may occur even after successful basic periodontal therapy, but it is small and limited to a small percentage of sites. Elevated inflammation markers of inflamed sites from disease patients reduced to the mean levels of those observed in healthy subjects after successful basic periodontal therapy. Significantly elevated both gene and protein levels of IL-10 in inflamed sites prior treatment confirms its modulatory role in the disease status.

The effect of nonsurgical periodontal therapy on hepcidin and on inflammatory and iron marker levels

Abstract Serum hepcidin levels may increase in response to infection and inflammation. The present study investigated the effect of nonsurgical periodontal therapy (NSPT) on levels of serum hepcidin, inflammatory markers, and iron markers. An interventional study was conducted on 67 patients (age 30-65 years) without other diseases, except for chronic periodontitis (CP). Patients were allocated to either CP or control groups. The CP group received supragingival and subgingival scaling and root planing procedures, whereas the control group received supragingival scaling. Probing depth (PD), bleeding on probing, clinical attachment level (CAL), visible plaque index (VPI), serum hepcidin and interleukin-6 (IL-6) levels, high-sensitivity C-reactive protein (hs-CRP), hematological markers, and iron markers were measured at baseline and at 90 days after NSPT. The CP group had statistically significant lower mean values for mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) (p ≤ 0.05). The control group had statistically significant reductions in hemoglobin, hematocrit, MCV, and MCH (p ≤ 0.05). Serum hepcidin, IL-6, and erythrocyte sedimentation rate (ESR) levels were significantly decreased in both groups after NSPT. Periodontal markers were more markedly reduced in the CP group compared with the control group (p ≤ 0.05). These findings suggest that NSPT may reduce the serum levels of IL-6, hepcidin, and periodontal parameters.

The Association Between Buccal Mucosa Thickness and Periimplant Bone Loss and Attachment Loss: A Cross-Sectional Study.

PURPOSE: The aim of this study was to assess if there is an association between buccal mucosa thickness and periimplant attachment loss after 1 year of function. MATERIALS AND METHODS: A total of 28 patients (14 periimplantitis implants and 14 healthy implants) were included. The buccal mucosal thickness was assessed using K-files at 3 mm apical to the soft tissue margin of the implant. Probing depth, recession (REC), clinical attachment level (CAL), bleeding on probing, and radiographic bone loss on mesial and distal sites of the implant were recorded. RESULTS: The data showed that there was a statistically significant difference in midfacial REC between thin and thick buccal mucosa groups. However, the CAL was not statistically significant different between both groups. In addition, there was no statistically significant difference in mesial and distal bone loss between implants with thin and thick mucosa. CONCLUSION: When the midfacial soft tissue thickness was thin, the midfacial REC was greater and the CAL also tended to be higher. There was no association between buccal mucosa thickness and periimplant bone loss on mesial and distal sites of the implant after 1 year of function.

Topical application of glycyrrhetinic acid in the gingival sulcus inhibits attachment loss in lipopolysaccharide-induced experimental periodontitis in rats.

BACKGROUND AND OBJECTIVE: Attachment loss of the junctional epithelium and alveolar bone destruction are signs of periodontitis, which is mainly caused by an inflammatory response to dental plaque. Glycyrrhetinic acid (GA), a component of the licorice herb, has been shown to have important anti-inflammatory activities; however, there are no previous reports on the ability of its inhibitory effects to prevent periodontal diseases. Hence, in this study, using our experimental periodontitis model, we attempted to evaluate whether GA had an effect on the prevention of attachment loss and alveolar bone loss. MATERIAL AND METHODS: Rats were intraperitoneally immunized with Escherichia coli lipopolysaccharide (LPS). The LPS group (n = 5) received 3 topical applications of 50 µg/µL of LPS followed by one application of the vehicle (propylene glycol:ethyl alcohol:phosphate-buffered saline [PBS] = 8:1:1) into the gingival sulcus. This protocol was repeated twice per day for 10 days. The low (n = 5) and high (n = 5) groups received topical application of LPS and 0.03% or 0.3% GA, respectively. The control group received topical application of PBS and vehicle. The rats were killed on the 10th day. Attachment loss, alveolar bone level and inflammatory cell infiltration were investigated histometrically. The formation of immune complexes and infiltration of LPS were evaluated immunohistologically. RESULTS: Attachment loss, formation of immune complexes and infiltration of inflammatory cells were increased in the LPS group compared with the control group, and were completely inhibited in the low and high groups compared with the LPS group. The LPS group showed greater alveolar bone destruction compared with the control group and GA-treated groups. In addition, invasion of LPS was detected in the LPS group, was absent in the control group and was weaker in the GA-treated groups than in the LPS group. CONCLUSION: In the present study, we showed that GA inhibits periodontal destruction in the rat experimental periodontitis model.

Clinical and radiographic periodontal parameters and release of collagen degradation biomarkers in naswar dippers.

BACKGROUND AND OBJECTIVE: The aim of the present study was to compare clinical periodontal parameters and to assess the release of C-telopeptides pyridinoline cross-links (ICTP) and C-terminal crosslinked telopeptide (CTX) from gingival collagen of naswar (NW) and non-naswar (control) dippers. MATERIAL AND METHODS: Eighty-seven individuals (42 individuals consuming NW and 45 controls) were included. Clinical (plaque index, bleeding on probing, probing depth and clinical attachment loss) and radiographic (marginal bone loss) periodontal parameters were compared among NW and control groups. Gingival specimens were taken from subjects in NW and control groups, assessed for ICTP and CTX levels (using ELISA) and analyzed using micro-Raman spectroscopy. The significance of differences in periodontal parameters between the groups was determined using Kruskal-Wallis and Mann-Whitney U tests. The percent loss of dry mass over exposure time and the rate of release of ICTP and CTX from all groups were compared using the paired t-test to examine the effects of exposure time. RESULTS: Clinical and radiographic periodontal parameters were significantly higher in the NW group than the control group (P < .01). In the Raman spectrum, the strongest and sharpest band occurred at 1260 cm-1 amongst NW users. A Raman band at Amide I was observed with slight shifts in wave numbers. The rate of ICTP and CTX release was significantly higher in subjects from the NW group compared with those from the control group (P < .05). Both factors, the type of groups and time, had a significant effect on release of ICTP and CTX (P < .05). CONCLUSION: Within the limits of the present study, it may be concluded that clinical and radiographic periodontal parameters were worse among subjects in the NW group than in those of the control group. There is a higher degree of collagen breakdown in the connective tissue of subjects in the NW group as a result of naswar usage.

Changes of Periodontal Parameters after Apical Surgery: Correlation of Clinical and Cone-beam Computed Tomographic Data.

INTRODUCTION: The purpose of this study was to evaluate the changes of the marginal periodontium 1 year after apical surgery. METHODS: Clinical and radiographic (cone-beam computed tomographic) examinations of 54 teeth treated with buccal access flaps for apical surgery were performed at baseline and after 1 year. Clinical assessment included measurements of probing pocket depth, the level of gingival margin (GM), and the width of keratinized tissue. Subsequently, the clinical attachment level (CAL) and the width of the attached gingiva were calculated. On bucco-oral cone-beam computed tomographic sections, the height and thickness of the crestal bone and the thickness of the alveolar bone were measured at different levels. RESULTS: In general, the calculated mean changes of periodontal tissue and crestal/alveolar bone were only minimal. Significant mean changes included only GM and CAL on midoral aspects and the distance from the cementoenamel junction or restoration margin on midbuccal sites. CAL was further correlated with the thickness of the alveolar bone at 3 mm below the cementoenamel junction or restoration margin. None of the clinically and radiographically calculated mean changes were correlated with sex, biotype, or incision techniques. With regard to age, older patients showed significantly more gingival recession on the buccal aspect compared with younger individuals. Furthermore, mean changes of the midbuccal width of the attached gingiva were positively correlated with the healing outcome, whereas mean changes of the midoral GM and CAL were negatively correlated with the healing outcome. CONCLUSIONS: Within an observation period of 1 year, the marginal periodontium and its underlying bone structures did not suffer from significant changes after apical surgery.

[How to analyze periodontal morphotypes in order to reduce the risk of periodontal recession]. / Savoir analyser le morphotype parodontal pour minimiser les risques de récessions parodontales.

INTRODUCTION: The periodontal morphotype is a leading feature to be born in mind during surgical, implant, prosthetic, restorative as well as orthodontic treatment. A fragile morphotype will rapidly trigger severe and worrying clinical repercussions for the patient. MATERIALS AND METHODS: In order to minimize the risks involved, sound knowledge of the different morphotypes and of the techniques for clinically evaluating them is a major requirement. These factors need to be regularly reassessed since morphotypes can vary throughout the course of treatment. RESULTS: Detecting and controlling mucogingival risk factors will enable an appropriate clinical approach designed to avoid the onset of secondary recessions or other gingival pathologies.

Effect of Helicobacter pylori infection on chronic periodontitis by the change of microecology and inflammation.

Helicobacter pylori (H. pylori), a pathogen inducing peptic disease, is recently found to be binding to the progress of periodontitis. Most previous studies are case-controlled, and they investigate the risk of H. pylori infection in disease the development of while few studies evaluate the correlation between H. pylori and periodontal pathogens. Therefore, we investigated the correlation between H. pylori infection with periodontal parameters, periodontal pathogens and inflammation. The results indicated that patients with H. pylori showed significantly higher probing depth and attachment loss than those without (p < 0.05). Among 28 subgingival plaque samples from 14 patients, the frequencies of Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum and Treponema denticola were significantly higher with H. pylori infection than those without H. pylori infection (p < 0.05). However, the frequency of Aggregatibacter actinomycetemcomitans was lower (p < 0.05). Furthermore, after human acute monocytic leukemia cell line (THP-1) was stimulated with cagA-positive standard strains (cagA+ H. pylori 26695), the expression of periodontitis-related molecules Wnt5a, interleukin 8 (IL-8), interleukin 6 (IL-6) and interferon gamma (IFN-γ) significantly increased (p < 0.05). Conversely, the expression of tumor necrosis factor alpha (TNF-α) was almost stable. Meanwhile, cagA+ H. pylori promoted significantly higher expression of IL-8 and Wnt5a than isogenic cagA mutants strains (cagA- H. pylori 26695) did. Taken together, our data suggested that H. pylori might promote the growth of some periodontal pathogens and aggravate the progress of chronic periodontitis.

Zirconia Dental Implants: Investigation of Clinical Parameters, Patient Satisfaction, and Microbial Contamination.

PURPOSE: In recent years, dental implants made from zirconia have been further developed and are considered a reliable treatment method for replacing missing teeth. The aim of this study was to analyze dental implants made from zirconia regarding their clinical performance compared with natural teeth (control). MATERIALS AND METHODS: One hundred six zirconia implants in 38 adults were analyzed in a clinical study after 1 year of loading. The plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD), probing attachment level (PAL), and creeping or recession (CR/REC) of the gingiva were detected and compared with natural control teeth (CT). Furthermore, the papilla index (PAP), Periotest values (PTV), microbial colonization of the implant/dental sulcus fluid, and patient satisfaction were assessed. RESULTS: The survival rate was 100%. No statistical significance was observed between implants and teeth regarding BOP, PPD, and PAL. A statistical significance was detected regarding PI and CR/REC with significantly less plaque accumulation and recession in the study group. Mean PAP was 1.76 ± 0.55, whereas the mean PTV was -1.31 ± 2.24 (range from -5 to +6). A non-statistically significant higher colonization of periodontitis/peri-implantitis bacteria was observed in the implant group. The questionnaire showed that the majority of the patients were satisfied with the overall treatment. CONCLUSION: One-piece zirconia dental implants exhibited similar clinical results (BOP, PPD, and PAL) compared with natural teeth in regard to adhesion of plaque (PI) and creeping attachment (CR/REC); zirconia implants performed even better. The favorable results for PAL and CR/REC reflect the comparable low affinity of zirconia for plaque adhesion. Patient satisfaction indicated a high level of acceptance for zirconia implants. However, a long-term follow-up is needed to support these findings.

Width of Keratinized Mucosa at Implant Sites in Patients Treated for Generalized Aggressive Periodontitis: A Cohort Study.

PURPOSE: The aim of this cohort study was to evaluate the width of keratinized mucosa at implant sites of partially edentulous patients who were treated for generalized aggressive periodontitis. MATERIALS AND METHODS: Dental implants were placed in 35 patients who were treated for generalized aggressive periodontitis and 18 periodontally healthy individuals (controls). At baseline, the keratinized mucosa of all implants was ≥ 2 mm. Follow-up examinations were conducted every 3 months over a 4-year period. RESULTS: The implant survival rate was 97.3% in patients with generalized aggressive periodontitis and 100% in the control group. Four years after implant insertion, patients with generalized aggressive periodontitis had significantly higher clinical attachment levels at the teeth and implants compared with the controls. At all time points, in both groups the mean probing depth at the implants was significantly larger than at the teeth. The mean widths of keratinized mucosa and keratinized gingiva were not significantly different between the two groups. In both groups, the widths of keratinized mucosa and keratinized gingiva were significantly higher at the maxilla than at the mandible. Four years after baseline, the implants in the mandible showed the smallest keratinized mucosa (mean: ≤ 1 mm). CONCLUSION: During the first 4 years after implant placement, no significant changes in the keratinized mucosa at implants could be shown, either in periodontally healthy patients or in patients treated for generalized aggressive periodontitis. The keratinized gingiva at the teeth was generally significantly wider than the keratinized mucosa at the implants.

Gingival crevicular fluid vascular endothelial cell growth factor and platelet-derived growth factor-BB release profile following the use of perforated barrier membranes during treatment of intrabony defects: a randomized clinical trial.

BACKGROUND AND OBJECTIVE: Perforated barrier membranes open channels between the suprabony and intrabony compartments of the defect, which could allow for more physiologic cellular interactions between different components of the periodontium during guided tissue regeneration surgery. To test this assumption, this study was designed to evaluate levels of vascular endothelial cell growth factor (VEGF) and platelet-derived growth factor (PDGF)-BB in gingival crevicular fluid during the early stages of healing of localized intrabony defects treated with perforated membranes (PMs) or non-PMs, as compared with open flap debridement. MATERIAL AND METHODS: Thirty non-smoking patients with severe chronic periodontitis participated in this prospective, randomized and single blinded trial. Each patient contributed one interproximal defect that was randomly assigned to the PM group (n = 10), occlusive membrane (OM) group (n = 10) or open flap debridement (OFD) group (n = 10). Plaque index, gingival index, probing depth, clinical attachment level and the intrabony depth of the defect were measured at baseline and reassessed at 6 and 9 mo after therapy. Gingival crevicular fluid samples were collected on days 1, 3, 7, 14, 21 and 30 d after therapy for the changes in VEGF and PDGF-BB levels. RESULTS: During the early stages of healing (1, 3 and 7 d), the mean VEGF and PDGF-BB concentrations at sites treated with PMs and OFD peaked with a statistically significant difference as compared with the OM-treated group. VEGF and PDGF-BB levels at sites treated with PMs and OFD were not statistically different. Growth factor levels decreased sharply in the samples obtained at days 21 and 30 with non-significant differences between the three groups. Nine months after therapy, the PM-treated group showed a statistically significant improvement in probing depth, clinical attachment level and intrabony defect compared to the OM and OFD groups. CONCLUSIONS: Within the limits of the present study, one can conclude that PM coverage of periodontal defects is associated with initial gingival crevicular fluid growth factor upregulation that could improve the clinical outcomes of guided tissue regeneration surgery.

Subgingival Microbial and Inflammatory Cell Morphotypes Associated with Chronic Periodontitis Progression in Treated Adults.

OBJECTIVE: In a secondary data analysis, this pilot study evaluated the relationship between subgingival biofilm morphotypes and chronic periodontitis progression in treated adults. METHODS: Periodontal parameters in 47 adults with chronic periodontitis were assessed by a calibrated examiner at baseline and a mean 4.5 years after a non-surgical periodontal therapy regimen. Microbial and inflammatory cell morphotypes in subgingival biofilm specimens from each patient were evaluated with phase-contrast microscopy at baseline, and at post-treatment intervals. Chronic periodontitis progression in patients was defined as ≥ 2 teeth exhibiting ≥ 3 mm interproximal clinical periodontal attachment loss from baseline evaluations. Bivariate and odds ratio analysis assessed baseline and post-treatment variables relative to chronic periodontitis progression. RESULTS: Eight (17%) patients had chronic periodontitis progression. No baseline clinical, radiographic or microbiological variables, and no post-treatment clinical variables demonstrated statistically significant relationships with chronic periodontitis progression. Elevated post-treatment counts of subgingival spirochetes, medium to large-sized motile rods, and crevicular leukocytes, both alone and concurrently, appeared more frequently in patients experiencing chronic periodontitis progression. A post-treatment occurrence of high concurrent counts of subgingival spirochetes and crevicular leukocytes exhibited the strongest association with chronic periodontitis progression (odds ratio = 10.1; 95% Cl = 2.2, 45.4; p = 0.004), which was greater than with either morphotype alone. CONCLUSIONS: Joint morphotype analysis of subgingival spirochetes and crevicular leukocytes, as simplified biomarkers of pathogenic biofilm infection and host inflammatory responses in periodontal pockets, may be diagnostically useful in assessing risk of progressive disease in treated chronic periodontitis patients.

Expression of cathepsin K in periodontitis and in gingival fibroblasts.

OBJECTIVE: To study non-osteoclastic sources of cathepsin K in periodontitis. MATERIALS AND METHODS: Tissue samples were obtained from 10 otherwise healthy periodontitis pati-ents during routine periodontal flap operations and 10 systemically and periodontally healthy individuals who underwent extraction operations for retained third molars. Methods used were immunohistochemistry, image analysis, immunofluorescence double-staining, gingival fibroblast culture, tumour necrosis factor-α (TNF-α) stimulation and Western blotting. RESULTS: Macrophage-like cells, fibroblast-like cells, vascular endothelial cells and gingival epithelial cells were more intensively stained for cathepsin K and also more frequent in periodontitis than in controls (665 ± 104 vs 258 ± 40 cells mm(-2) , P < 0.01). Some cathepsin K(+) cells in periodontal tissues were CD68(+) , but some were CD68(-) and probably fibroblasts. Indeed, in gingival fibroblast culture, resting fibroblasts released cathepsin K, more 43 kD procathepsin K than 29 kD active cathepsin K. TNF-α increased the release of the activated cathepsin K 4- to 5-fold. CONCLUSIONS: Results suggest that GCF-cathepsin K is not only osteoclast-derived, but in periodontitis, also other cells contribute to it. GCF-cathepsin K, perhaps together with intracellular, lysosomal collagenolytically active cathepsin K in fibroblasts, macrophages and gingival epithelial cells, can contribute to the loss of attachment and destruction of the periodontal ligament.