Effect of the pro-resolution lipid mediator Resolvin E1 (RvE1) on pulp tissues exposed to the oral environment.

AIM: To evaluate the effects of topical Resolvin E1 (RvE1) application on infected dental pulps. METHODOLOGY: Forty-two male Wistar rats (n = 6 per three groups/and two time periods) were used. To induce inflammation, pulps in mandibular right first molars were accessed and then left exposed to the oral environment for 24 h. After this period, topical medication with a corticosteroid/antibiotic blend, or RvE1, or its vehicle (Ethanol 0.1%) was directly applied onto the pulp tissue and teeth were restored with silver amalgam. The effects of the protocols were evaluated histologically and compared with control pulps not exposed to the oral environment. The inflammatory changes after 24 and 72 h were assessed through a scoring method and analysed using the Kruskal-Wallis test followed by Dunn's. Differences were considered significant if P < 0.05 (CI = 95%). RESULTS: Ethanol and corticosteroid/antibiotic treatment were not effective in arresting severe inflammatory alterations of exposed pulps at 24 and 72 h (P < 0.05, CI = 95%). At both time periods, RvE1 treatment led to a reduction of tissue cellularity and extent of inflammation, whose changes were not different from control pulps (P > 0.05, CI = 95%). CONCLUSIONS: A protective role for RvE1 in pulp inflammation was observed even in the presence of contamination, suggesting that it may be a candidate for a novel therapeutic strategy for conservative dental pulp treatment.

Purine nucleoside phosphorylase activity and expression are upregulated in sites affected by periodontal disease.

BACKGROUND AND OBJECTIVE: Purine nucleoside phosphorylase (PNP) is an enzyme that catalyzes the reversible phosphorolysis of purine nucleosides, playing a key role in the purine salvage pathway. Activated T cells seem to rely heavily on PNP to remain functionally active and are particularly sensitive to PNP deficiency. The role of PNP in periodontal tissues has not been characterized thus far. The aim of this study therefore was to assess the activity and expression of PNP in the gingival tissues of periodontitis patients. MATERIAL AND METHODS: Ten patients consecutively admitted for treatment had their periodontal clinical variables recorded and their gingival crevicular fluid collected. After periodontal treatment the patients were seen once a month for plaque and bleeding control, and had their periodontal variables recorded and gingival crevicular fluid collected at 90 and 180 d. Purine nucleoside phosphorylase-specific activity was assessed using a spectrophotometer through the addition of the PNP substrate analog 2-amino-6mercapto-7-methyl purine riboside to the gingival crevicular fluid. In parallel, PNP expression was assessed by immunohistochemistry and real-time PCR in gingival biopsies and cell culture. RESULTS: Purine nucleoside phosphorylase activity was higher in the gingival crevicular fluid of periodontally diseased sites, which was positively correlated with improvements of the clinical variables. Treatment of periodontal disease induced a striking decrease of PNP activity in periodontally diseased sites. Expression of PNP was more pronounced in mononuclear cells and endothelial cells of the gingiva, and the mRNA levels were 5.7-fold higher in inflamed tissues compared with control samples. CONCLUSION: Purine nucleoside phosphorylase activity and expression are upregulated in periodontally diseased sites and can be detected in the gingival crevicular fluid.

Moesin-induced signaling in response to lipopolysaccharide in macrophages.

BACKGROUND AND OBJECTIVE: Many physiological and pathophysiological conditions are attributable in part to cytoskeletal regulation of cellular responses to signals. Moesin (membrane-organizing extension spike protein), an ERM (ezrin, radixin and moesin) family member, is involved in lipopolysaccharide (LPS)-mediated events in mononuclear phagocytes; however, its role in signaling is not fully understood. The aim of this study was to investigate the LPS-induced moesin signaling pathways in macrophages. MATERIAL AND METHODS: Macrophages were stimulated with 500 ng/mL LPS in macrophage serum-free medium. For blocking experiments, cells were pre-incubated with anti-moesin antibody. Moesin total protein and phosphorylation were studied with western blotting. Moesin mRNA was assessed using quantitative real-time PCR. To explore binding of moesin to LPS, native polyacrylamide gel electrophoresis (PAGE) gel shift assay was performed. Moesin immunoprecipitation with CD14, MD-2 and Toll-like receptor 4 (TLR4) and co-immunoprecipitation of MyD88-interleukin-1 receptor-associated kinase (IRAK) and IRAK-tumor necrosis factor receptor-activated factor 6 (TRAF6) were analyzed. Phosphorylation of IRAK and activities of MAPK, nuclear factor kappaB (NF-kappaB) and IkappaBalpha were studied. Tumor necrosis factor alpha, interleukin-1beta and interferon beta were measured by ELISA. RESULTS: Moesin was identified as part of a protein cluster that facilitates LPS recognition and results in the expression of proinflammatory cytokines. Lipopolysaccharide stimulates moesin expression and phosphorylation by binding directly to the moesin carboxyl-terminus. Moesin is temporally associated with TLR4 and MD-2 after LPS stimulation, while CD14 is continuously bound to moesin. Lipopolysaccharide-induced signaling is transferred downstream to p38, p44/42 MAPK and NF-kappaB activation. Blockage of moesin function interrupts the LPS response through an inhibition of MyD88, IRAK and TRAF6, negatively affecting subsequent activation of the MAP kinases (p38 and ERK), NF-kappaB activation and translocation to the nucleus. CONCLUSION: These results suggest an important role for moesin in the innate immune response and TLR4-mediated pattern recognition in periodontal disease.

Management of soft tissue ridge deformities with acellular dermal matrix. Clinical approach and outcome after 6 months of treatment.

BACKGROUND: Soft tissue ridge defects often hamper ideally shaped artificial crowns and are basically treated using autogenous soft tissue grafts or alloplastic materials. These approaches present disadvantages such as the necessity of creating additional surgical fields to harvest the graft and the requirement of primary closure, which may reduce ridge height. This investigation evaluated the use of acellular dermal matrix (ADM) in the treatment of soft tissue ridge defects. METHODS: Eight patients, non-smokers with non-contributory medical history, provided 18 sites corresponding to missing teeth in the anterior maxillary arch. The ideal horizontal gain (desired gain) was waxed up in study casts, which served as templates for construction of modified acrylic stents with orthodontic wires. These stents served as references for ideal horizontal gain and also as fixed reference points for further evaluation. The distance from the orthodontic wire to the buccal plate of the defect also represented its baseline horizontal component. Vertical variations were evaluated with another stent and, in this case, no desired gain was considered. After raising partial-thickness flaps, the ADM material was rehydrated and folded to fill the defect and reproduce the desired gain. Flaps were sutured with no tension, and part of the material was intentionally left exposed to avoid pressure on the incision line and prevent height loss. Patients used local and systemic antimicrobials, and the sutures were removed at 7 days. RESULTS: Evaluations were carried out at 30 days, and 3 and 6 months, and all sites healed uneventfully. Neither infection nor significant pain was reported by the patients, and the material was covered by tissue at about 21 days. Mean horizontal gain of 1.72 +/- 0.59 mm (58.5%) at 6 months and mean shrinkage of 1.22 +/- 0.46 mm (41.4%) were observed. There was a mean improvement in vertical gain of only 0.61 +/- 0. 77 mm, although 66. 7% of the treated sites showed a 1 to 2 mm gain. Clinically, the total gain in the subjects was very effective and matched the receptor tissues nicely. CONCLUSIONS: ADM may be a suitable material for the treatment of soft tissue ridge deformities due to its biocompatibility, color matching, and horizontal gain. Additional controlled, comparative trials are necessary to establish its advantages and potential compared to autogenous soft tissue techniques.

Managing soft tissue fenestrations in bone grafting surgery with an acellular dermal matrix: a case report.

The success of bone grafting procedures depends largely on the management and integrity of the gingival flaps. Soft tissues aid in the protection of the bone graft, participate in the revascularization of the newly formed hard tissues, and play an important role in the esthetic outcome of the reconstructive phase. Acellular dermal matrix (ADM) is a material obtained from human skin and used in plastic and reconstructive surgery as an allograft. It acts as a bioactive substrate for cell attachment and proliferation. The outcome of the use of ADM as a dressing material to treat flap fenestrations in bone grafting surgery is presented.

Guided tissue regeneration associated with bovine-derived anorganic bone in mandibular class II furcation defects. 6-month results at re-entry.

BACKGROUND: The use of graft materials with guided tissue regeneration (GTR) in Class II furcation defects is aimed at improving the outcome of the regenerative technique. In this regard, however, there are a limited number of studies discussing the results obtained when GTR and graft materials are used in the treatment of Class II furcation defects. Furthermore, most studies employ either allogeneic or autogenous materials. The present trial sought to determine whether the use of a bovine-derived anorganic bone (ABB) in conjunction with GTR influenced the outcome of mandibular Class II furcation treatment. METHODS: This study included 14 patients who provided 15 pairs of similar periodontal defects. Each defect was randomly assigned to treatment with either a cellulose membrane in combination with bovine-derived anorganic bone (GTR+ABB) or membrane alone (GTR). Following basic therapy, baseline measurements were recorded including probing depth (PD), clinical attachment level (CAL), and gingival margin position (GMP). Hard tissue measurements were performed during surgery to determine alveolar crestal height (CEJ-AC), and vertical (VDD) and horizontal defect depth (HDD). Membranes remained in position for at least 4 weeks. After 6 months, all sites were re-entered and soft and hard tissue measurements were recorded. RESULTS: Both surgical procedures resulted in statistically significant probing depth reduction and gain in clinical attachment levels, with no significant difference between groups. Gingival recession was more pronounced in the GTR+ABB group (0.87 +/- 0.83 mm), but not statistically different from the GTR group (0.46 +/- 1.19 mm). Vertical defect resolution was significant in both groups (GTR: 1.60 +/- 1.50 mm; GTR+ABB: 1.80 +/- 2.11 mm), without differences between groups. Only horizontal furcation resolution (GTR: 2.47 +/- 0.99 mm; GTR+ABB: 3.27 +/- 1.39 mm) was significantly different between groups (P <0.05). CONCLUSIONS: The use of ABB with GTR techniques improved horizontal defect resolution in mandibular Class II furcation defects, but did not yield superior results regarding soft tissue changes when compared to sites treated with GTR alone. Evaluation of a larger sample could indicate differences and advantages between the evaluated approaches and confirm the real necessity of associating filling materials with GTR.

Use of bovine-derived anorganic bone associated with guided tissue regeneration in intrabony defects. Six-month evaluation at re-entry.

BACKGROUND: Different filling materials have been associated with guided tissue regeneration (GTR) in order to improve its regenerative potential and predictability. Anorganic bovine bone (ABB) has demonstrated biocompatibility and osteoconductive properties; however, there are limited data regarding its performance in the treatment of intrabony defects. This investigation aimed to evaluate the clinical outcome of the association of anorganic bovine bone with cellulose membranes in intrabony defects after 6 months. METHODS: Twenty-six paired intrabony defects were selected from 11 non-smoking patients with no relevant medical history. The defects were similar regarding the number of bony walls and defect depth, and presented pocket depths > or = 6 mm. Four weeks after completion of basic therapy, probing depth (PD), clinical attachment level (CAL), and gingival margin position (GP) were recorded (baseline values). The defects were then surgically accessed and debrided, and the intrabony component measured to the nearest millimeter with periodontal probes and customized acrylic stents (distance from the stent to the base of the defect and from the stent to the alveolar crest). Each intrabony defect was randomly assigned to receive the membrane alone (control, C) or the membrane with anorganic bovine bone (test, T). The patients were re-evaluated after 6 months, and re-entry procedures were performed. RESULTS: Significant (P <0.01) improvement in all variables was observed: mean pocket reduction of 4.61+/-1.60 mm (C) and 4.46+/-1.50 mm (T) and clinical attachment gain of 2.85+/-1.46 mm (C) and 3.15+/-1.40 mm (T); the difference between groups was not significant (P >0.05). Nevertheless, gingival recession in the control group (1.84+/-0.89 mm) was significantly (P <0.05) more pronounced than that observed in the test group (1.30+/-0.48 mm). Bone measurements indicated a significant resolution of the defects (P <0.01). A mean defect resolution of 2.76+/-0.72 mm (C) and 2.69+/-1.03 mm (T) and crestal resorption of 1.07+/-0.64 mm (C) and 1.30+/-0.85 mm (T) were detected (P >0.05). Stepwise multiple regression analysis indicated that for both groups, the baseline depth of the defects and the alveolar crest resorption accounted for 82% of the variability of bone fill observed in the control group (F = 23.65, P <0.001) and 89% in the test group (F = 41.32, P <0.001). CONCLUSIONS: ABB may be used in conjunction with GTR in the treatment of intrabony defects. Its use, however, did not result in a better outcome than the use of membranes alone. Studies employing more patients would be of interest in order to determine the advantages and indications of the tested approaches on a more predictable basis.

Necrotizing ulcerative periodontitis associated with severe congenital immunodeficiency in a prepubescent subject: clinical findings and response to intravenous immunoglobulin treatment.

Common variable immunodeficiency (CVID) is a rare multifactorial congenital disease of genetic origin caused by an impairment in the secretion of specific immunoglobulins. It manifests systemically through recurrent respiratory infections, gastrointestinal disorders and autoimmune diseases. Oral manifestations may include gingivitis and lichenoid lesions with Wickham's striae. The treatment for CVID is supported by using intravenous infusion of immunoglobulins (IVIG) that allows for control of the disease and avoidance of recurrent opportunistic infections. This report presents a case of necrotizing ulcerative periodontitis (NUP) in a young patient with CVID, and correlates his periodontal status with systemic conditions before and after IVIG administration during 1 year of evaluation.

Manifestations of insulin-dependent diabetes mellitus in the periodontium of young Brazilian patients. A 10-year follow-up study.

Eight female and 3 male patients from a group of 30 patients studied 10 years earlier and who had received no periodontal treatment during this period, in order to evaluate the progression of untreated periodontal disease in patients with insulin-dependent diabetes mellitus, were evaluated in terms of plaque accumulation, gingival inflammation, probing depth, and alveolar bone loss. The total number of dental surfaces that presented clinically detectable plaque deposits increased significantly (29% to 43%; P < 0.01; chi 2 = 46.36). Site-specific comparisons for plaque index between studies showed a significant variation (P < 0.01) in the upper arch only for palatal surfaces and in the lower arch for the buccal and lingual surfaces. The total dental surfaces with inflamed surrounding gingiva increased from 11% to 33% in this study (P < 0.01; chi 2 = 175.78). Site-specific comparison for gingival index showed a significant variation for all upper surfaces, while such difference for the lower arch was significant only for the buccal and lingual surfaces. The arithmetic means for the probing depth for the upper buccal, upper palatal, lower buccal, and lower lingual surfaces increased significantly (P < 0.01). The arithmetic means of alveolar bone loss also increased significantly for the upper posterior and lower regions (P < 0.01) and for the upper anterior and lower anterior regions (P < 0.05). The correlation between age and probing depth was significant only for the upper palatal region (P < 0.01). The correlation between age and bone loss was significant only for the upper posterior region (P < 0.05). The results of this follow-up study suggest that despite little variation in plaque accumulation, gingival inflammation, probing depth, and bone loss increased after a 10-year interval in patients who had received no periodontal treatment during this period.