Use of 17% EDTA as an Adjunct in Management of Class I Recession with Semilunar Coronally Advanced Flap - A Case Report

Gingival recession is usually characterized by the apical displacement of the gingival margin, exposing the root surface when related to cemento-enamel junction. It has turned out to be one of the most common perturbations for the patients, apart from esthetic, root sensitivity, progression of periodontal diseases and root caries are the major fields of concern. The goal of periodontist is not only to treat gingival recession but also to rectify the functional and esthetic deficiencies to further combat the periodontal destruction. Semilunar flap is one of the procedures followed to cover recession, being a simple, minimally invasive and effective technique with higher patient acceptance and provides satisfactory results for Miller’s class I recession. Semilunar flap when combined with EDTA, as root conditioner provides a biocompatible cell surface for tissue attachment. Here we are presenting a case report where semilunar coronally advanced flap was used for treatment of Miller’s Class I recession in maxillary central incisor. Keywords: EDTA, Esthetics, Gingival Recession, Semilunar Flap.

Astaxanthin Inhibits Diabetes-Triggered Periodontal Destruction, Ameliorates Oxidative Complications in STZ-Injected Mice, and Recovers Nrf2-Dependent Antioxidant System

Numerous studies highlight that astaxanthin (ASTX) ameliorates hyperglycemic condition and hyperglycemia-associated chronic complications. While periodontitis and periodontic tissue degradation are also triggered under chronic hyperglycemia, the roles of ASTX on diabetes-associated periodontal destruction and the related mechanisms therein are not yet fully understood. Here, we explored the impacts of supplemental ASTX on periodontal destruction and systemic complications in type I diabetic mice. To induce diabetes, C57BL/6 mice received a single intraperitoneal injection of streptozotocin (STZ; 150 mg/kg), and the hyperglycemic mice were orally administered with ASTX (12.5 mg/kg) (STZ+ASTX group) or vehicle only (STZ group) daily for 60 days. Supplemental ASTX did not improve hyperglycemic condition, but ameliorated excessive water and feed consumptions and lethality in STZ-induced diabetic mice. Compared with the non-diabetic and STZ+ASTX groups, the STZ group exhibited severe periodontal destruction. Oral gavage with ASTX inhibited osteoclastic formation and the expression of receptor activator of nuclear factor (NF)-κB ligand, 8-OHdG, γ-H2AX, cyclooxygenase 2, and interleukin-1β in the periodontium of STZ-injected mice. Supplemental ASTX not only increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and osteogenic transcription factors in the periodontium, but also recovered circulating lymphocytes and endogenous antioxidant enzyme activity in the blood of STZ-injected mice. Furthermore, the addition of ASTX blocked advanced glycation end products-induced oxidative stress and growth inhibition in human-derived periodontal ligament cells by upregulating the Nrf2 pathway. Together, our results suggest that ASTX does not directly improve hyperglycemia, but ameliorates hyperglycemia-triggered periodontal destruction and oxidative systemic complications in type I diabetes.

Age-dependent Oral Manifestations of Neurofibromatosis Type 1: A Case-control Study

Introduction: Craniofacial manifestations of neurofibromatosis type 1 (NF1) are considered as a result of tumor compression. We sought to determine age-dependent salivary changes, carious, and periodontal complications in NF1 patients without tumors in the oral cavity.Objective and methods: Eleven NF1 patients without tumors in the oral cavity and 29 matched controls without NF1 were enrolled in this case-control study. Demographic information, medical history, and data of intraoral examinations, including the Decayed, Missing, and Filled Teeth (DMFT) scores and Russel’s periodontal index (PI), were recorded. The functional salivary analysis was performed for sialometry, salivary pH values, and amylase activity. Ingenuity Systems Pathway Analysis (IPA) was conducted to identify mutually activated pathways for NF1-associated oral complications.Results: NF1 patients were associated with periodontitis (OR=1.40, 95% CI=1.06-1.73, P = 0.04), gingivitis (OR=1.55, 95% CI=1.09-2.01, P = 0.0002), and decreased salivary flow rate (OR=1.40, 95% CI=1.05-1.76, P = 0.005). Periodontal destruction, salivary changes, and dental caries in NF1 patients were age dependent. Subgroup analyses based on age stratification suggested that salivary flow rates and salivary amylase activity were significantly lower among NF1 patients aged over 20 years and that salivary pH values, PI and DMFT scores were higher among NF1- controls aged over 20. All oral complications were not significantly presented among NF1 patients aged below 20. IPA analyses suggested that cellular mechanisms underlying NF1-associated oral complications involved chronic inflammatory pathways as well as fibrosis signalling pathway.Conclusion: NF1 patients without tumors in the oral cavity presented with a higher prevalence of age-dependent oral complications, including periodontal destruction and salivary gland dysfunction, which were associated with chronic inflammatory pathogenesis.

Inflamm-Aging-Related Cytokines of IL-17 and IFN-γ Accelerate Osteoclastogenesis and Periodontal Destruction

Periodontal disease (PD), as an age-related disease, prevalent in middle-aged and elderly population, is characterized as inflammatory periodontal tissue loss, including gingival inflammation and alveolar bone resorption. However, the definite mechanism of aging-related inflammation in PD pathology needs further investigation. Our study is aimed at exploring the effect of inflamm-aging-related cytokines of interleukin-17 (IL-17) and interferon-γ (IFN-γ) on osteoclastogenesis in vitro and periodontal destruction in vivo. For receptor activator of nuclear factor-κB ligand- (RANKL-) primed bone marrow macrophages (BMMs), IL-17 and IFN-γ enhanced osteoclastogenesis, with the expression of osteoclastogenic mRNA (TRAP, c-Fos, MMP-9, Ctsk, and NFATc1) and protein (c-Fos and MMP-9) upregulated. Ligament-induced rat models were established to investigate the role of IL-17 and IFN-γ on experimental periodontitis. Both IL-17 and IFN-γ could enhance the local inflammation in gingival tissues. Although there might be an antagonistic interaction between IL-17 and IFN-γ, IL-17 and IFN-γ could facilitate alveolar bone loss and osteoclast differentiation.

Aggregatibacter actinomycetemcomitans- A periodontopathogen

is a gram-negative oral pathobiont that is associated with severe form of periodontitis. This bacterium has various virulence factors which enables the bacterium to colonize the oral cavity, invade and evade the host defences. Leukotoxin and cytolethal distending toxin are the important virulence factors that causes periodontal destruction. Periodontal infections with seems to be refractory to conventional therapy and systemic antibiotics. Hence, leukotoxin represents an ideal anti-virulence target and inhibition of its immunosuppressive activity would eliminate the colonization advantage provided to the bacteria by the toxin. This review provides a comprehensive update of with an emphasis on its virulence factors leukotoxin and cytolethal distending toxin and its role in periodontal destruction and recent developments in the management.

Rare Genetic Disorders Affecting the Periodontal Supporting Tissues in Adolescence

In adolescents periodontal destruction may be the primary manifestation of an as yet unrecognized rare systemic disease, and it may be up to the periodontist to make the correct tentative diagnosis. Many genetic diseases that present with primary periodontal manifestations in adolescence affect immune function, sometimes with only mild or absent systemic features. They include periodontal Ehlers-Danlos syndrome (lack of attached gingiva, various connective tissue abnormalities), Papillon-Lefèvre syndrome (palmoplantar hyperkeratosis), and plasminogen deficiency (fibrin deposition within mucous membranes). Other immune disorders with severe periodontitis manifesting in adolescence are usually diagnosed in early childhood due to unmistakeable systemic features. They include Cohen syndrome (developmental disorder, truncal obesity, and microcephaly), Hermansky-Pudlak Syndrome (oculocutaneous albinism, bleeding diathesis, and other systemic manifestations), glycogen storage disease type 1b, and Chediak-Higashi syndrome (pyogenic infections, albinism, and neuropathy). The structural integrity of periodontal tissue is affected in genodermatoses such as Kindler syndrome, a type of epidermolysis bullosa. In primary hyperoxaluria, inflammatory periodontal destruction is associated with renal calculi. Breakdown of periodontal tissues independent of dental plaque biofilm-induced periodontitis is found in hypophosphatasia (highly variable skeletal hypomineralization) or isolated odontohypophosphatasia, hypophosphatemic rickets and primary hyperparathyroidism. Finally, alveolar osteolysis mimicking localized periodontitis may be due to neoplastic processes, e.g., in neurofibromatosis type 1 (typical skin features including café au lait macules and neurofibromas), Langerhans cell histiocytosis (locally destructive proliferation of bone marrow-derived immature myeloid dendritic cells), and Gorham-Stout disease (diffuse cystic angiomatosis of bone).

Effect of Cigarette Smoking on Periodontal Status of Diabetic Patients

Background: Periodontitis is an inflammatory disease of the tooth-supporting structures that can lead to periodontal destruction and tooth loss. It is also a common complication of diabetes mellitus (DM) and tobacco smoking. In this regard, this study aimed to assess the effect of smoking on periodontal disease in diabetic patients. Methods: This case-control study was conducted on 80 diabetic patients who were referred to the clinics of the Department of Periodontics of Ardabil University of Medical Sciences from October 2015 to April 2016. Participants were enrolled in this study in four groups (n=20). Groups 1 and 2 included smoker diabetic patients and 20 non-smoker diabetics, respectively. In addition, groups 3 and 4 served as the control groups and included healthy smoker and non-smoker individuals, respectively. The plaque index (PI), clinical probing depth (CPD), clinical attachment level (CAL), and bleeding on probing (BOP) were measured in the four groups. Results: The four groups were significantly different regarding the PI and CPD (P<0.05). The mean PI was higher in group 1 compared to groups 2 and 3. The highest mean CAL was recorded in group 1. Finally, non-diabetic smokers experienced the lowest mean BOP compared with other groups. Conclusion: DM and tobacco smoking are the known major risk factors for periodontal disease, and the interaction effect of the two factors can aggravate the periodontal status in diabetic patients. Thus, dentists can take an important step in the healthcare system by encouraging their patients to control their DM and quit smoking.

Patterns of Periodontal Destruction among Smokeless Tobacco Users in a Central Indian Population

Background: Findings of studies testing the association between smokeless tobacco (SLT) use and periodontal health have shown varying results in different populations. Considering the high prevalence of SLT use in India, the present study was conducted to understand the pattern of periodontal destruction within different areas of the dentition among SLT users. Methods: Age, gender, oral hygiene habits, the frequency and duration of SLT consumption, the type of SLT product used, and the site of retention of the SLT product in the oral cavity were recorded among 90 SLT users. Probing depth (PD), recession (REC), and clinical attachment loss (CAL) at SLT-associated and non SLT-associated teeth of the mandibular arch were compared based on the site of retention of the SLT product, the type of product used, and the duration of the habit. Results: REC and CAL were significantly higher at the SLT-associated zones compared to non SLT-associated zones and at both interproximal and mid-buccal sites of SLT-associated teeth. Among individuals who had the habit for more than 5 years and also among those who had the habit for 5–10 years, PD, REC, and CAL were significantly higher at SLT-associated teeth than at non SLT-associated teeth. Significantly greater periodontal destruction was observed at SLT-associated teeth among khaini users and gutkha users. Conclusions: Smokeless tobacco consumption resulted in greater destruction of periodontal tissues. The severity of periodontal destruction at SLT-associated sites differed depending on the type of smokeless tobacco used, the site of retention of the SLT, and the duration of the habit.