Gingival crevicular fluid levels of monocyte chemoattractant protein-1 in periodontal health and disease

Objectives

Monocyte chemoattractant protein-1 (MCP-1) stimulates the chemotaxis of monocytes and also several cellular events associated with chemotaxis thus causes recruitment of inflammatory cells. Its increased gingival crevicular fluid (GCF) levels in periodontal disease have been reported in previous studies. The present study has been carried out to assess the role of MCP-1 in periodontal disease progression and also to determine the effect of periodontal treatment on MCP-1 concentration in GCF.

Design

A total of 60 subjects were divided into three groups (n = 20) based on gingival index (GI), probing pocket depth (PPD) and clinical attachment loss (CAL): healthy (group I), gingivitis (group II) and chronic periodontitis (group III). A fourth group (group IV) consisted of 20 subjects from group III, 6-8 weeks after treatment (i.e. scaling and root planing). GCF samples collected from each patient were quantified for MCP-1 using ELISA.

Results

The mean MCP-1 concentration in GCF was found to be the highest in group III, i.e. 72.60 pg/μl. The mean MCP-1 concentration in group I was 19.70 pg/μl and in group IV was 8.50 pg/μl. The mean MCP-1 concentration (37.00 pg/μl) in group II was found to lie in between the concentrations obtained in groups I and III.

Conclusions

GCF MCP-1 levels increased progressively with the progression of disease and decreased after treatment. Levels of MCP-1 correlated positively with clinical parameters like GI, PPD and CAL thus it can be considered as an inflammatory biomarker in periodontal disease and also deserves further consideration as a therapeutic target.     

Effect of nonsurgical periodontal therapy on crevicular fluid levels of Cathepsin K in periodontitis

Objectives

Cathepsin K (CTSK), predominantly expressed in osteoclasts, is a potent extracellular matrix degrading enzyme that plays a critical role in osteoclast-mediated bone resorption. Its increased gingival crevicular fluid (GCF) levels in periodontal disease have been reported in a previous study. The present study has been carried out to assess the role of CTSK in periodontal disease and to determine the effect of periodontal treatment on CTSK concentration in GCF.

Design

60 subjects were divided into three groups (n = 20) based on gingival index (GI), probing pocket depth (PPD) and clinical attachment loss (CAL): healthy (group I), gingivitis (group II) and chronic periodontitis (group III). A fourth group (group IV) consisted of 20 subjects from group III, 6-8 weeks after nonsurgical periodontal therapy (scaling and root planing). GCF samples collected from each patient were quantified for CTSK using ELISA.

Results

The mean CTSK concentration in GCF was found to be the highest in group III, i.e. 55.55 pmol/l. The mean CTSK concentration in GCF in group I and group II was 5.95 pmol/l and 6.90 pmol/l respectively. The mean CTSK concentration in GCF in group IV decreased to 11.15 pmol/l, slightly more than that in groups I and II.

Conclusions

GCF CTSK levels increased in periodontitis and correlated negatively with clinical parameters like GI, PPD and CAL. CTSK levels decreased after nonsurgical treatment of periodontitis. Thus, CTSK can be considered as a ‘marker of osteoclastic activity’ in periodontal disease and also deserves further consideration as a therapeutic target.     

GCF and serum myeloperoxidase and matrix metalloproteinase-13 levels in renal transplant patients

Aim

The rationale of this study was to address whether local or systemic changes reflect proteolytic (matrix metalloproteinase-13) or oxidative (myeloperoxidase) stress in renal transplant patients receiving cyclosporine-A (CsA) and having gingival overgrowth (GO), in patients receiving CsA therapy and having no GO and patients receiving tacrolimus therapy.

Material and methods

Gingival crevicular fluid (GCF) samples were collected from sites with (GO+) and without GO (GO−) in CsA patients having GO; GO− sites in CsA patients having no GO; sites from tacrolimus, gingivitis and healthy subjects. GCF and serum myeloperoxidase (MPO) and matrix metalloproteinase-13 (MMP-13) levels were determined by ELISA.

Results

GO+ sites in CsA patients having GO had elevated GCF MPO levels than those of CsA patients having no GO, tacrolimus and healthy subjects (p < 0.005), but comparable to those of gingivitis. GCF MPO levels were higher in GO+ compared to GO− sites in CsA patients having GO (p < 0.05). Patient groups had similar, but higher GCF MMP-13 levels than healthy group.

Conclusions

These results show that CsA and tacrolimus therapy have not a significant effect on GCF MPO and MMP-13 levels, and gingival inflammation seems to be the main reason for their elevations.     

Crevicular fluid levels of plasma glutathione peroxidase (eGPx) in periodontal health and disease

Background & objectives

Reactive oxygen species (ROS) have been implicated in numerous human diseases, including periodontal diseases. Plasma glutathione peroxidase (eGPx) as an important antioxidant, has a protective role against ROS and is an established marker of oxidative stress. The present study evaluated the levels of eGPx in GCF to further probe into the role of oxidants and antioxidants in periodontal disease.

Methods

60 subjects were divided into three groups consisting of 20 subjects in each group based on gingival index, pocket probing depth, clinical attachment loss and radiological parameters (bone loss): healthy (group 1), gingivitis (group 2) and periodontitis (group 3), whilst, group 3 patients after the treatment constituted group 4. GCF samples were collected from all groups to estimate the levels of eGPx using ELISA.

Results

The mean eGPx concentration in GCF were observed to be the highest in group 3 i.e., 30.89 ± 4.93 ng/μl and lowest in group 1 i.e., 15.32 ± 3.06 ng/μl. The mean eGPx concentration in group 2 (23.77 ± 2.91 ng/μl) and group 4 (18.92 ± 3.53 ng/μl) fell between the highest and the lowest values.

Conclusion

This suggests that eGPx levels in GCF increase proportionally with the severity of periodontal diseases. eGPx can be considered as a marker of oxidative stress in periodontal diseases. However, controlled, longitudinal studies with larger samples have to be carried out to confirm this possibility.     

Effect of nifedipine on gingival enlargement and periodontal breakdown in ligature-induced periodontitis in rats

Objective

A recent consensus report could not find specific reports of the effect of nifedipine on the destruction of the periodontal tissues. The aim of the present study was to evaluate the effect of nifedipine on gingival enlargement and periodontal breakdown using a ligature-induced periodontitis in rats.

Materials and methods

Fifty, male, 60 days old, Wistar rats, were divided into six groups. Cotton sutures were placed around the upper second molars. Two groups of 10 rats each did not receive ligatures and were treated daily with either saline solution or nifedipine 50 mg/kg/day. Two groups of 10 rats received ligatures and were also treated daily with saline solution or nifedipine 50 mg/kg/day. Two additional groups (nifedipine 10 and 100 mg/kg/day) were included to explore a possible dose-response relationship. Animals were euthanatised at 30 days. Internal and oral epithelium, total and inflamed connective tissue, gingival thickness and height, and bone loss were assessed histologically.

Results

Nifedipine alone was not sufficient to promote gingival enlargement or periodontal destruction in the absence of the ligature. Compared to animals with ligatures only, the group that received ligatures and nifedipine 50 mg/kg/day showed significant higher estimates for total and inflamed connective tissue, gingival thickness and height. No significant differences were observed for bone loss between these experimental groups. The other dosages of nifedipine did not provide additional information.

Conclusion

Nifedipine itself did not lead to gingival enlargement in rats. In the presence of biofilm accumulation, nifedipine yielded greater gingival enlargement and periodontal inflammation, but it did not increase periodontal destruction.     

Prevalence and distribution of serotype-specific genotypes of Aggregatibacter actinomycetemcomitans in chronic periodontitis Brazilian subjects

Objective

Previous studies have suggested that Aggregatibacter actinomycetemcomitans is involved in the aetiology of aggressive periodontitis as well as chronic periodontitis. In addition, some authors have also reported that serotype-specific antigens of A. actinomycetemcomitans determine the severity of disease. This study aimed to elucidate the prevalence of A. actinomycetemcomitans and the distribution of A. actinomycetemcomitans serotypes in Brazilian subjects with chronic periodontitis.

Design

A total of 486 individuals were enrolled in this survey. All patients received clinical examinations that included periodontal pocket depth, clinical attachment loss, plaque, and gingival indexes. Subgingival samples were taken for microbial analysis. The genomic DNA of A. actinomycetemcomitans was provided by PCR.

Results

Out of 486 subjects examined, A. actinomycetemcomitans was isolated in 85 (17.5%) individuals. Out of 85 positive samples, 68 were infected by at least 1 serotype, 7 by mixed infection, and 10 were non-serotyped. Serotypes d and f were not detected. Serotype c showed the highest prevalence (52.9%), followed by serotype a (31.8%).

Conclusions

Intragroup analysis revealed that, in slight/moderate periodontitis, serotypes c and a were significantly more prevalent than serotypes b and d-f; the prevalence of serotype c in severe periodontitis was significantly greater than that of serotypes a and b. Our data were similar in Asian and Eurasian populations.     

Differential gene and protein expression of tissue inhibitors of metalloproteinases (TIMP)-3 and TIMP-4 in gingival tissues from drug induced gingival overgrowth

Objectives

The purpose of this study was to analyse mRNA expression and protein localization of tissue inhibitors of metalloproteinases (TIMP)-3 and TIMP-4 in gingival tissues removed from drug (calcium-channel blocker) induced gingival overgrowth and periodontitis patients.

Design

Employing RT-PCR, we evaluated TIMP-3 and TIMP-4 mRNA levels of 20 human gingival tissue samples taken from patients suffering gingival overgrowth (GO) and periodontitis (P). Then, using immunohistochemistry we investigated the TIMP-3 and TIMP-4 protein localization of five sample tissues from each group.

Results

TIMP-4 mRNA levels in GO-gingiva tended to be lower than in P-gingiva but the results differed little (p = 0.22). Varying degrees of inflammation in the protein localization of TIMP-3 and TIMP-4 were found. TIMP-4 immunoreactivity (IR) was weak in the endothelial cells, fibroblasts, epithelial basal and parabasal cells while the degree of inflammation differed as well. TIMP-3 and TIMP-4 IR in inflammatory cells, including lymphocytes, plasma cells, and macrophages, were faint and intense respectively. For P-gingiva, both TIMP-3 and TIMP-4 IR expression was weak in the endothelial cells, fibroblasts, basal and parabasal epithelial layers. Expression of TIMP-3 was faint in the inflammatory cells, whereas TIMP-4 IR was strong.

Conclusion

Our findings suggest that TIMP-3 and TIMP-4 expression differs in GO and P-gingival tissues, both of which are potentially involved in pathogenesis.     

Influence of glycemic control on Epstein-Bar and Cytomegalovirus infection in periodontal pocket of type 2 diabetic subjects

Objective

The aim of the present study was to evaluate the influence of glycemic control on the frequency of Epstein-Bar (EBV) and Cytomegalovirus (CMV) in periodontal pockets of type 2 diabetic subjects with chronic periodontitis.

Design

Forty-six subjects presenting generalized chronic periodontitis and type 2 diabetes mellitus (DM) were selected for this study. Polymerase chain reaction (PCR) was used to determine the presence of EBV and CMV in shallow [Probing Depth (PD) ≤ 3 mm], moderate (PD = 4-6 mm) and deep (PD > 7 mm) pockets. HbA1c levels ≤7%, >7 to <10%, and ≥10% defined good, moderate and poor glycemic control, respectively.

Results

Higher frequency of EBV was found in the shallow pockets of the subjects with poor glycemic control (p < 0.05; chi-square test). Moreover, EBV-free subjects presented moderate or good glycemic control. Glycemic control did not influence the frequency of CMV in all pocket categories.

Conclusion

Poor glycemic control in type 2 diabetic subjects can increase the occurrence of EBV in shallow periodontal pockets.     

Expression of HMGB1 and HMGN2 in gingival tissues, GCF and PICF of periodontitis patients and peri-implantitis

Background and objective

High mobility group chromosomal protein B1 (HMGB1) and N2 (HMGN2), two members of high mobility group (HMG) family, play important role in inflammation. The purpose of this study was to investigate the expression of HMGB1 and HMGN2 in periodontistis.

Materials and methods

The expression of HMGB1 and HMGN2 mRNA in gingival tissues and gingival crevicular fluid (GCF) in chronic periodontitis (CP), generalised aggressive periodontitis (G-AgP) patients and healthy subjects was detected by real-time PCR. The protein level of HMGB1 and HMGN2 in peri-implant crevicular fluid (PICF), peri-implant crevicular fluid of peri-implantitis (PI-PICF) and normal patients was determined by Western blotting. Furthermore, IL-1β, IL-6, IL-8, TNF-α and HMGB1 levels in GCF, PI-PICF and healthy-PICF samples from different groups were determined by ELISA.

Results

HMGN2 expression was increased in inflamed gingival tissues and GCF from CP and G-ApG groups compared to control group. HMGB1 expression was the highest in the gingival tissues and GCF from CP patients and was accompanied by increased concentrations of IL-1β, IL-6, IL-8 proinflammaory cytokines.

Conclusion

To our knowledge, this is the first study reporting that the expression of HMGB1 and HMGN2 was increased in the gingival tissues and GCF in CP and G-AgP and the PICF in PICF. Our data suggest that HMGB1 may be a potential target for the therapy of periodontitis and PI.     

Midkine expression in human periapical granulomas

Introduction

The expression of midkine (MK), a heparin-binding growth factor, is increased in various human tumors, making it a promising tumor marker and target for tumor therapy. MK is also related to the regulation of the development and etiology of chronic or autoimmune diseases; however, the involvement of MK in apical periodontitis has never been examined. This study compared the localization of MK-expressing cells and MK messenger RNA expression in periapical granulomas with healthy gingival tissues.

Methods

Periapical lesions were removed surgically from chronic apical periodontitis patients, and serial tissue sections were stained with hematoxylin-eosin. The lesions diagnosed as periapical granulomas pathologically were examined by immunohistochemistry using human MK monoclonal antibodies. MK messenger RNA expression was also detected using real-time polymerase chain reaction analysis. Healthy gingival tissues were analyzed in the same manner.

Results

MK was expressed by inflammatory cells, such as macrophages, lymphocytes, and neutrophils, as well as by endothelial cells in periapical granulomas but not in healthy gingival tissues. The MK-expressing inflammatory cells were seen adjacent to blood vessels, which contained MK-expressing endothelial cells, suggesting the interaction of MK among these cells during the process of inflammatory cell infiltration. Quantitative analysis of MK messenger RNA expression revealed that periapical granulomas expressed significantly more MK than healthy gingival tissues.

Conclusions

These findings suggest that MK is involved in the pathogenesis of periapical granulomas.     

Angiotensin-converting enzyme (ACE), angiotensinogen (AGT), and angiotensin II type 1 receptor (AT1R) gene polymorphisms in generalized aggressive periodontitis

Aim

Host response to periodontopathic microorganisms can be modulated by genetic factors. Accumulated evidence highlighted the role of renin-angiotensin system (RAS) in inflammatory response thus potential implication of this molecular system in the pathogenesis of periodontitis can be suggested. The present study investigated common genetic variants of molecules within the RAS family namely angiotensin-converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II type 1 receptor (AT1R) in relation to generalized aggressive periodontitis (G-AgP).

Methods

DNA was obtained from peripheral blood of 103 G-AgP patients and 100 periodontally healthy subjects. ACE I/D, AGT M235T and AT1R A1166C polymorphisms were genotyped by polymerase chain reaction and restriction fragment length polymorphism method. Chi-square, ANOVA and logistic regression were used in statistical analyses.

Results

Both ACE I/D and AT1R polymorphisms were similar in G-AgP and healthy groups (p > 0.05). G-AgP subjects exhibited decreased AGT TT genotype and T allele frequency as compared to healthy subjects (p < 0.05). The same trend was also observed in the nonsmoker subgroup regarding investigated RAS polymorphisms.

Conclusions

Present findings suggest that AGT M235T TT genotype and T allele might be associated with decreased risk for G-AgP in Turkish population.     

Increase of gingival matured dendritic cells number in elderly patients with chronic periodontitis

Objective

The purpose of this study was to evaluate the inflammatory cell subset proportions in the upper gingival connective tissue, including mature dendritic cells (DC) in elderly and younger patients with generalized chronic periodontitis in order to further understand the effect of aging on gingival inflammatory phenomenon.

Methods

Gingival tissue specimens presenting chronic periodontitis from 8 elderly patients aged >75 (test group, group T) and from 8 younger patients aged 50-60 (considered as controls, group C) were analysed by immunohistochemistry using monoclonal antibodies against CD45RB, CD4, CD8, CD19, CD68, DC-SIGN, DC-LAMP molecules. The number of each immunolabelled cells subset was counted using image analysis.

Results

The difference in the number of CD45RB + leucocytes in the upper gingival connective tissue between groups was not significant permitting to use it as reference. As compared to group C, the lymphocyte subsets/CD45RB + leucocytes ratios tended to decrease in group T but the decrease was significant only for CD4 + T lymphocytes/CD45RB + cells ratio (p < 0.03). On the opposite, the ratios of antigen-presenting cells DC-SIGN + cells/CD45RB + cells and DC-LAMP + cells/CD45RB + cells were significantly increased (p < 0.03 and <0.0001, respectively) in group T. Moreover, in group T the DC-LAMP + cells/DC-SIGN + cells ratio was significantly increased (p < 0.05) showing an increased number of matured dendritic cells.

Conclusion

During chronic periodontitis in elderly patients, our results show a decrease in the ratio of gingival CD4 + lymphocyte subset associated with an increase in the ratios of antigen-presenting cells subsets and more particularly maturated DC-LAMP + dendritic cells.     

Imbalance of oxidative/anti-oxidative status induced by periodontitis is involved in apoptosis of rat submandibular glands

Objective

Epidemiologic studies suggest a relationship between periodontitis and salivary gland dysfunction. A rat periodontitis model was used to investigate whether a causal relationship exists between periodontitis and pathological changes of submandibular glands.

Design

Fourteen male Wistar rats (8 weeks old) were divided into two groups (n = 7/group): a control group and periodontitis group. Periodontitis was induced by ligature placement around the mandibular first molars. Serum levels for reactive oxygen metabolites, anti-oxidant and tumour necrosis factor (TNF)-α were measured at baseline, 2 and 4 weeks. At 4 weeks, the levels of 8-hydroxydeoxyguanosine were determined to evaluate oxidative damage of submandibular glands. Expression of TNF-α mRNA and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL) as well as histological findings were also evaluated in the submandibular glands.

Results

The rats with experimental periodontitis showed increase in the levels of serum reactive oxygen metabolites and TNF-α, and a decrease of anti-oxidant power in a time-dependent manner. At 4 weeks, these rats also had significantly increased levels of 8-hydroxydeoxyguanosine and TNF-α, and increased number of TUNEL-positive cells and vacuolisation in the submandibular glands compared to the control rats.

Conclusions

Imbalance of circulating oxidative/anti-oxidative status may be involved in vacuolisation and apoptosis of submandibular glands in the rat periodontitis model.     

The role of Desulfovibrio desulfuricans lipopolysaccharides in modulation of periodontal inflammation through stimulation of human gingival fibroblasts

Objective

Periodontitis is a destructive disease which is likely to be the result of the activities of different microbial complexes. Recently, sulphate-reducing bacteria (SRB) have been detected in the oral cavity, and they have been found to be common inhabitants of sites showing periodontal destruction. The aim of study was to evaluate the influence of endotoxins of Desulfovibrio desulfuricans bacteria on human gingival fibroblast HGF-1 line.

Methods

The immunological response of gingival fibroblasts was evaluated by determination of their IL-6 and IL-8 secretion upon treatement with D. desulfuricans intestinal and type strain LPS, sodium butyrate (NaB) and IL-1β. The amounts of cytokines were estimated by ELISA immunoassay. The influence of LPS and NaB on fibroblast proliferation was determined using the CyQUANT Cell Proliferation Assay Kit.

Results

No significant growth inhibition of cells exposed to LPS was observed, except for the culture growing in the presence of intestinal strain endotoxin at the highest concentration (100 μg/ml). The secretion of IL-6 and IL-8 by fibroblasts was increased by D. desulfuricans endotoxins. Cells stimulated with proinflammatory cytokine 1L-1β showed very high levels of both cytokines secretion. The release of IL-6 and IL-8 by cells in response to LPS and 1L-1β was modulated by butyric acid.

Conclusions

The observed response of gingival fibroblasts to stimulation by endotoxin suggests that D. desulfuricans can be involved in the pathogenesis of periodontitis. Moreover, butyrate present in the oral cavity seems to have immunoregulatory effect on cytokine production by gingival fibroblasts under physiological conditions and during microbe-induced inflammation.     

Relationship between smoking and endodontic variables in hypertensive patients

Introduction

The aim of this study was to investigate the relationship between smoking and the prevalence of apical periodontitis and root canal treatment in hypertensive patients.

Methods

In a cross-sectional study, the records of 100 hypertensive patients, 50 smokers and 50 nonsmokers, were examined. Periapical status of all teeth was assessed by using the periapical index score.

Results

Apical periodontitis in 1 or more teeth was found in 92% of smoker patients and in 44% of nonsmoker subjects (P = .000; odds ratio [OR], 16.8; 95% confidence interval [CI], 4.6-61.3). One or more root-filled teeth were found in 58% and 20% of smoker and nonsmoker subjects, respectively (P < .01; OR, 5.5; 95% CI, 2.3-13.5). Among smoker hypertensive patients, 6% of the teeth had apical periodontitis, whereas in the nonsmoker subjects, 2% of teeth were affected (P < .01; OR, 3.3; 95% CI, 2.0-5.4). The percentage of root-filled teeth in the smoker and nonsmoker groups was 3.6% and 1.2%, respectively (P < .01; OR, 2.9; 95% CI, 1.6-5.5).

Conclusions

The prevalence of apical periodontitis and root canal treatment was significantly higher in smoker hypertensive patients compared with nonsmoker subjects.     

Receptor for advanced glycation end products (RAGE)-expressing endothelial cells co-express AGE and S100 in human periapical granulomas

Objective

The engagement of the receptor for advanced glycation end products (RAGE) by AGE or S100 perturbs homeostatic mechanisms and provides a basis for cellular dysfunction in pathological situations. To assess the mechanism of vascular immune reactions in chronic periapical periodontitis, we analysed co-expression of RAGE and AGE or S100 in periapical granulomas.

Methods

Surgically removed periapical lesions, which had been diagnosed as chronic periodontitis, were inspected histologically using paraffin-embedded sections stained with haematoxylin and eosin. Cryostat sections of the tissues, which were identified histologically as periapical granulomas, were then examined by double immunohistochemistry using polyclonal antibodies raised against human CD34 and monoclonal antibodies specific for human RAGE, AGE or S100. Dual-colour immunofluorescence image analysis was also performed to assess the co-expression of RAGE and AGE or RAGE and S100 by endothelial cells.

Results

Marked expression of RAGE, AGE, and S100 by CD34⁺ endothelial cells was noted. Dual-colour immunofluorescence image analysis revealed that the RAGE-expressing endothelial cells co-expressed AGE and S100; however, the number of RAGE-AGE-expressing endothelial cells was significantly higher than that of RAGE-S100-expressing endothelial cells.

Conclusions

Co-expression of RAGE and AGE by endothelial cells in periapical granulomas is more relevant than that of RAGE and S100. The possible engagement of RAGE and AGE may trigger cellular activation and mediate tissue injury.     

Human β-defensin 2 and protease activated receptor-2 expression in patients with chronic periodontitis

Objective

Some previous studies have shown that gingipains, trypsin-like proteases produced by Porphyromonas gingivalis, up-regulate human β defensin-2 (HBD-2) mRNA expression through protease-activated receptor-2 (PAR₂) in gingival epithelial cells. This study aimed at investigating salivary HBD-2 levels and crevicular PAR₂ mRNA expression in human chronic periodontitis and evaluating whether periodontal treatment affected this process.

Methods

Salivary and gingival crevicular fluid (GCF) samples were collected from periodontally healthy (control) and chronic periodontitis patients at baseline and 50 days after non-surgical periodontal treatment. Salivary HBD-2, and GCF TNF-α levels were analysed by ELISA, and PAR₂ mRNA at the GCF was evaluated by RT-PCR.

Results

P. gingivalis was significantly (p < 0.05) more prevalent in patients with chronic periodontitis when compared to controls. This prevalence decreased after periodontal therapy (p < 0.0001). The control group showed statistically significant lower levels of HBD-2, TNF-α, and PAR₂ expression when compared to the chronic periodontitis group. In addition, periodontal treatment significantly reduced PAR₂ expression and HBD-2 levels in chronic periodontitis patients (p < 0.001).

Conclusions

Our results suggest that salivary HBD-2 levels and PAR₂ mRNA expression from GCF are higher in subjects with chronic periodontitis than in healthy subjects, and that periodontal treatment decreases both HBD-2 levels and PAR₂ expression.     

Comparative evaluation of platelet-rich plasma and guided tissue regeneration membrane in the healing of apicomarginal defects: a clinical study

Introduction

The aim of the study was to compare the healing responses of platelet-rich plasma (PRP), PRP + a collagen sponge, and a collagen membrane used as guided tissue regeneration (GTR) materials for the treatment of apicomarginal defects.

Methods

Thirty patients with suppurative chronic apical periodontitis and apicomarginal communication were selected and allocated randomly into three groups according to the barrier technique to be used during periradicular surgery: the collagen membrane group, the PRP group, and the PRP + collagen sponge group. Clinical and radiographic measurements were determined at baseline and every 3 months after surgery up to 1 year. Cases were defined as healed when no clinical signs or symptoms were present, and radiographs showed complete or incomplete (scar tissue) healing of previous radiolucencies.

Results

The PRP and PRP + collagen sponge groups depicted 83.33% and 88.89% healing, respectively, in terms of combined clinical-radiographic healing as compared with 80% in the collagen membrane group. All the three treatments showed highly significant (P < .05) reductions in the periodontal pocket depth (PD), the clinical attachment level (CAL), the gingival margin position (GMP), the size of the periapical lesion, the percentage reduction of the periapical rarefactions, and periapical healing. No significant differences between the three groups were evident for these parameters (P > .05).

Conclusions

GTR applied to apicomarginal defects using PRP or PRP + collagen sponge lead to similar enhancements of the clinical outcome of periradicular surgery in terms of periapical healing, gain of periodontal support, PD reduction, and PRP may be an alternative treatment for GTR membrane in the treatment of apicomarginal defects.     

Presence and quantification of mast cells in the gingiva of cats with tooth resorption, periodontitis and chronic stomatitis

Objective

Mast cells are tissue-dwelling granule-containing immune cells that play a pivotal role in the pathogenesis of inflammation and other processes. The three most common orodental disorders in cats are periodontitis, feline resorptive lesions (FRL), and chronic gingivostomatitis (FCGS). The presence and density of mast cells in the gingiva has been established in healthy cats but not in cats affected by FRL, FCGS or periodontitis. The aim of the present study was to document and quantify the presence of mast cells in the gingiva adjacent to teeth affected by FRL, FCGS or chronic periodontitis.

Methods

Samples from the gingiva of 32 cats affected by FRL, FCGS or periodontitis were obtained and compared to samples obtained from 7 specific pathogen-free (SPF) cats. Evaluation of mast cells and the inflammatory infiltrate were performed on hematoxylin and eosin, and toluidine blue stained sections.

Results

Mast cells densities were significantly increased in gingival tissues adjacent to teeth affected by FRL, FCGS or periodontitis in comparison to SPF samples. There were no significant differences between gingival tissues of the FRL, FCGS and periodontitis groups. However, the relative inflammatory score in the FRL group was significantly lower as compared to the FCGS or periodontitis groups, yet with similar density of mast cells.

Conclusion

In the gingiva of cats affected with FRL, FCGS or periodontitis, there is an increase in the number of mast cells. The high number of mast cells in the FRL group and concurrent mild inflammatory reaction suggests the notion that mast cells may potentially play role in the pathogenesis of FRL.     

A single application of hydrogen sulphide induces a transient osteoclast differentiation with RANKL expression in the rat model

Objective

Oral malodor is mainly attributed to volatile sulphur compounds (VSCs) such as hydrogen sulphide (H₂S), methyl mercaptan and dimethyl sulphide. VSC accelerate periodontal soft tissue destruction. However, there is little information about the potential role of H₂S in alveolar bone loss. The purpose of this animal study was to examine the effects of sodium hydrogen sulphide (NaHS), H₂S donor drug, on osteoclast differentiation in rat periodontal tissue.

Design

Twenty-four male Wistar rats (8 weeks old) were divided into four groups: a control group and three experimental groups, which were examined at 3 h, 1 day, and 3 days after topical application of 3 μl NaHS (l M in physiological saline) into the gingival sulcus of rat first molar. Expression of tumour necrosis factor (TNF)-α, RANKL, NF-κB and tartrate-resistant acid phosphatase (TRAP) was evaluated in the periodontal tissue.

Results

Three hours after NaHS application, TNF-α expression increased in the periodontal ligament. The numbers of RANKL-positive osteoblasts and TRAP-positive osteoclasts significantly increased progressively with time and reached a maximum level after 1 day. Significant up-regulation of RANKL and NF-κB mRNA was observed at 3 h after NaHS application.

Conclusions

H₂S application caused a transient increase of osteoclast differentiation with up-regulation of RANKL expression in osteoblasts. H₂S, which is primarily responsible for halitosis, may also contribute to alveolar bone resorption through RANKL expression.