Periodontal Inflammatory Conditions Research Articles

Influence of mechanical debridement with adjunct probiotic therapy on clinical status and salivary cortisol levels in patients with periodontal inflammation.

The null hypothesis is that there is no difference in periodontal parameters and salivary cortisol levels (CL) among patients with periodontal inflammatory conditions (PIC) who receive non-surgical mechanical debridement (NSMD) with or without adjunct probiotic therapy (PT). The aim of this study was to assess the influence of NSMD with and without adjunct PT on clinical status and whole salivary CL in patients with PIC. Participants were randomly divided into four groups: Group-1: NSMD alone (n=19); Group-2: NSMD + PT (n=18); Group-3: PT + oral hygiene instructions (OHI) (n=17); and Group-4: PT alone (n=18). Lactobacillus rhamnosus SP1 (2×107 colony-forming units/day) was used for PT. Plaque and gingival indices (PI and GI), probing depth (PD) and clinical attachment loss (AL) were assessed, and whole salivary CL was assessed at baseline and at 6-week follow-up. Marginal bone levels were assessed at baseline and demographic data was collected using a questionnaire. Sample-size estimation was performed, and statistical significance was determined at p<0.05. At follow-up, PI (p<0.01), GI (p<0.01), and PD (p<0.01) were significantly higher in PT + OHI and PT alone groups compared with individuals who underwent NSMD + PT and NSMD alone. At baseline and follow-up, there was no significant difference in CL in all groups. There was no statistically significant correlation between age, gender, PI, PD, GI, clinical AL, salivary flow rate, education status and salivary CL in all groups at baseline and follow-up. NSMD continues to be the "gold standard" and most reliable treatment strategy for managing PIC. It is imperative to reach a consensus regarding the duration, dosage, and frequency of PT that would yield optimal results for managing PIC.

SOCS2 regulates alveolar bone loss in Aggregatibacter actinomycetemcomitans-induced periodontal disease.

The role of suppressor of cytokine signaling 2 (SOCS2) in Aggregatibacter actinomycetemcomitans (Aa)-induced alveolar bone loss is unknown; thus, it was investigated in this study. Alveolar bone loss was induced by infecting C57BL/6 wild-type (WT) and Socs2-knockout (Socs2-/-) mice with Aa. Bone parameters, bone loss, bone cell counts, the expression of bone remodeling markers, and cytokine profile were evaluated by microtomography, histology, qPCR, and/or ELISA. Bone marrow cells (BMC) from WT and Socs2-/- mice were differentiated in osteoblasts or osteoclasts for analysis of the expression of specific markers. Socs2-/- mice intrinsically exhibited irregular phenotypes in the maxillary bone and an increased number of osteoclasts. Upon Aa infection, SOCS2 deficiency resulted in the increased alveolar bone loss, despite decreased proinflammatory cytokine production, in comparison to the WT mice. In vitro, SOCS2 deficiency resulted in the increased osteoclasts formation, decreased expression of bone remodeling markers, and proinflammatory cytokines after Aa-LPS stimulus. Collectively, data suggest that SOCS2 is a regulator of Aa-induced alveolar bone loss by controlling the differentiation and activity of bone cells, and proinflammatory cytokines availability in the periodontal microenvironment and an important target for new therapeutic strategies. Thus, it can be helpful in preventing alveolar bone loss in periodontal inflammatory conditions.

Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review.

Periodontitis is a periodontal inflammatory condition that results from disrupted periodontal host-microbe homeostasis, manifested by the destruction of tooth-supporting structures, especially inflammatory alveolar bone loss. Osteoporosis is characterized by systemic deterioration of bone mass and microarchitecture. The roles of many systemic factors have been identified in the pathogenesis of osteoporosis, including endocrine change, metabolic disorders, health-impaired behaviors and mental stress. The prevalence rate of osteoporotic fracture is in sustained elevation in the past decades. Recent studies suggest that individuals with concomitant osteoporosis are more vulnerable to periodontal impairment. Current reviews of worse periodontal status in the context of osteoporosis are limited, mainly centering on the impacts of menopausal and diabetic osteoporosis on periodontitis. Herein, this review article makes an effort to provide a comprehensive view of the relationship between osteoporosis and periodontitis, with a focus on clarifying how those risk factors in osteoporotic populations modify the alveolar bone homeostasis in the periodontitis niche.

Oral Senescence: From Molecular Biology to Clinical Research

Cellular senescence is an irreversible cell cycle arrest occurring following multiple rounds of cell division (replicative senescence) or in response to cellular stresses such as ionizing radiation, signaling imbalances and oxidative damage (stress-induced premature senescence). Even very small numbers of senescent cells can be deleterious and there is evidence that senescent cells are instrumental in a number of oral pathologies including cancer, oral sub mucous fibrosis and the side effects of cancer therapy. In addition, senescent cells are present and possibly important in periodontal disease and other chronic inflammatory conditions of the oral cavity. However, senescence is a double-edged sword because although it operates as a suppressor of malignancy in pre-malignant epithelia, senescent cells in the neoplastic environment promote tumor growth and progression. Many of the effects of senescent cells are dependent on the secretion of an array of diverse therapeutically targetable proteins known as the senescence-associated secretory phenotype. However, as senescence may have beneficial roles in wound repair, preventing fibrosis and stem cell activation the clinical exploitation of senescent cells is not straightforward. Here, we discuss biological mechanisms of senescence and we review the current approaches to target senescent cells therapeutically, including senostatics and senolytics which are entering clinical trials.

Comparative evaluation of periodontal inflammatory conditions among gutka-chewers with and without prediabetes.

The metabolic syndrome has become one of the major public-health challenges worldwide which include diabetes, prediabetes (raised blood glucose level), abdominal obesity, high cholesterol level, and high blood pressure. Periodontitis is described as a multi-factorial irreversible and cumulative condition and, is also the sixth complication of diabetes. Areca nut chewing has already been linked with the development of various cancers, and more recently with metabolic syndrome. Therefore, the purpose of the study is to investigate the association of periodontal inflammatory conditions among gutka chewing with and without prediabetes patients. There are about 50 pre-diabetic and 50 healthy patients, both males and females with the age range of 18 years to 45 years, were included in the study. They were then divided into 4 groups based upon gutka chewers and non-chewers i.e., pre-diabetic gutka chewers (PDC), pre-diabetic non-chewers (PDNC), healthy gutka chewers (HC), and healthy non-chewers (HNC). A complete demographic data was obtained along with clinical and radiographic parameters i.e. plaque index (PI), sulcus bleeding index (SBI), probing depth (PD), marginal bone loss (MBL) were recorded. A statistical analysis was performed and Bonferroni adjustment post hoc test was performed for multiple comparisons. The overall results suggested that the clinical periodontal parameters i.e., PD, PI, SBI and radiologic parameters i.e., MBL are significantly higher in prediabetes chewers compared with healthy chewers and healthy non chewers. The periodontal inflammatory conditions are worse in gutka chewers compared to non-chewers in healthy and pre-diabetic patients, concluding that the severity of periodontal inflammation is governed by hyperglycemia when compared to habitual gutka usage.

Low association between bleeding on probing propensity and the salivary aMMP-8 levels in adolescents with gingivitis and stage I periodontitis.

Bleeding on probing (BOP) is a widely accepted measure used in periodontal diagnostics. Previous studies suggest that several factors can affect BOP propensity. The aim of this study was to investigate the relative impact of different local and modifying factors on BOP levels. The oral health of five hundred and forty-four adolescents (two birth cohorts) aged 15-17years living in Kotka, Finland, was examined including periodontal probing depth, visible plaque index, root calculus, and BOP. Whole saliva samples were collected and measured for active matrix metalloproteinase-8 (aMMP-8) by time-resolved immunofluorometric assay (IFMA). Bacterial plaque/calculus accumulation (oral hygiene) had a major influence on BOP levels. The relative impact was several times greater compared with the extent of periodontal pocketing, aMMP-8 levels, smoking, toothbrushing, or gender. Furthermore, BOP levels were significantly elevated among adolescents with poor oral hygiene than good oral hygiene even if adjusted for the extent of periodontal pocketing (P<.001). BOP levels could be low even if several≥4mm deep periodontal pockets existed. The difference in the extent of periodontal pocketing was not significant between the two birth cohorts of adolescents (P=.731). BOP levels can be regarded as an important indicator of the extent of bacterial challenge and its adverse effects on the gingival inflammation. However, the level of oral hygiene may mask the association between the extent of gingival bleeding and the severity of the periodontal inflammatory condition. Thus, relying on BOP levels (below 10% or 20%) may provide insufficient information about the periodontal treatment need of an adolescent depending on his/her level of oral hygiene. Yet, more research is needed to confirm the results, also in adult populations.

Alkaline Phosphatase Levels Before and After Nonsurgical Periodontal Therapy

Introduction: Chronic periodontitis is a multifactorial disease resulting in the inflammation and destruction of the supporting structures. Early detection of periodontal changes, prognosis and efficacy of treatment have been monitored by Alkaline Phosphatase Levels (ALP) levels.&#x0D; Objective: This study was carried out to determine level of ALP in saliva and serum before and after periodontal therapy.&#x0D; Methods: This pretest posttest study included 22 patients with generalised chronic periodontitis (GCP). The patients received nonsurgical periodontal therapy (NSPT). Saliva and serum levels of ALP were measured at baseline and after two months of periodontal therapy.&#x0D; Results: Twenty-two patients of mean age 44 years were analysed. Participants had significantly better periodontal parameters after two months. Salivary ALP levels, which were high at baseline, decreased after periodontal treatment. A significant positive correlation (0.0001) was found between the salivary levels of ALP and periodontal inflammatory conditions. Gingival index was found directly proportional with salivary ALP level but not with serum ALP.&#x0D; Conclusion: Periodontal therapy lowered the levels of ALP saliva in GCP patients with high ALP levels. Biochemical analysis of enzymes found in saliva may help in patients’ evaluation to determine the control and progression of periodontal destruction and aid in a correct diagnosis, prognosis and, consequently, better treatment.

Histone Methylation Mechanisms Modulate the Inflammatory Response of Periodontal Ligament Progenitors.

Inflammatory conditions affect periodontal ligament (PDL) homeostasis and diminish its regenerative capacity. The complexity of biological activities during an inflammatory response depends on genetic and epigenetic mechanisms. To characterize the epigenetic changes in response to periodontal pathogens we have focused on histone lysine methylation as a relatively stable chromatin modification involved in the epigenetic activation and repression of transcription and a prime candidate mechanism responsible for the exacerbated and prolonged response of periodontal cells and tissues to dental plaque biofilm. To determine the effect of inflammatory conditions on histone methylation profiles, related gene expression and cellular functions of human periodontal ligament (hPDL) progenitor cells, a hPDL cell culture system was subjected to bacterial cell wall toxin exposure [lipopolysaccharide (LPS)]. Chromatin immunoprecipitation-on-chip analysis revealed that healthy PDL cells featured high enrichment levels for the active H3K4me3 mark at COL1A1, COL3, and RUNX2 gene promoters, whereas there were high occupancy levels for the repressive H3K27me3 marks at DEFA4, CCL5, and IL-1β gene promoters. In response to LPS, H3K27me3 enrichment increased on extracellular matrix and osteogenesis lineage gene promoters, whereas H3K4me3 enrichment increased on the promoters of inflammatory response genes, suggestive of an involvement of epigenetic mechanisms in periodontal lineage differentiation and in the coordination of the periodontal inflammatory response. On a gene expression level, LPS treatment downregulated COL1A1, COL3A1, and RUNX2 expression and upregulated CCL5, DEFA4, and IL-1β gene expression. LPS also greatly affected PDL progenitor function, including a reduction in proliferation and differentiation potential and an increase in cell migration capacity. Confirming the role of epigenetic mechanisms in periodontal inflammatory conditions, our studies highlight the significant role of histone methylation mechanisms and modification enzymes in the inflammatory response to LPS bacterial cell wall toxins and periodontal stem cell function.

Effects of tofacitinib on the clinical features of periodontitis in patients with rheumatoid arthritis: two case reports

BackgroundThe pathobiology of rheumatoid arthritis (RA) is similar to that of periodontitis in that proinflammatory cytokines play an important pathologic role. There is evidence to suggest that inhibitors of tumor necrosis factor (TNF) and interleukin-6 (IL-6) receptor for the treatment of RA ameliorated periodontal inflammation. However, no study has evaluated the effect of tofacitinib, an oral Janus kinase inhibitor for the treatment of RA, on periodontitis.Case presentationThe present report cases are 51- and 43-year-old non-smoking women with RA who demonstrated localized moderate chronic periodontitis. Both cases showed improvement in the periodontal inflammatory condition after 3 months of tofacitinib therapy, although the teeth count and supragingival bacterial plaque level were relatively unchanged. Improvements were also observed in the serum levels of IL-6 in both cases as well as in the serum levels of TNF-α and anti-cyclic citrullinated peptide immunoglobulin G in one case and of rheumatoid factor and matrix metalloproteinase-3 in the other case. Patients who received tofacitinib exhibited an inconsistent clinical response, likely due to the low disease activity of RA at the start of the administration.ConclusionsThese are the first reported cases in which tofacitinib may have a beneficial effect on periodontitis. However, more research is required to understand the relationship between periodontitis and tofacitinib therapy.

Salivary Interleukin 1-beta levels and clinical periodontal parameters in habitual naswar users and non-users.

Objectives:Aim of our study was to assess the expression of salivary Interleukin 1-beta (IL-1β) and clinical periodontal parameters in naswar users and non-users (controls).Methods:Eighty four individuals (forty-two naswar users and forty-two controls) were included in the study which was conducted between August 2017 and May 2018. Salivary IL-1β levels, plaque index (PI), bleeding on probing (BOP), probing depth (PD) and clinical attachment loss (CAL) was assessed in all the participants.Results:PD of 4mm (p<0.05), PD of 5-6mm (p<0.05), CAL (p<0.001) and levels of salivary IL-1β (p<0.05) were significantly higher among naswar users as compared to controls while PI, BOP and number of missing teeth showed no significant difference among the two groups (p>0.05).Conclusion:Periodontal inflammatory conditions were worse and salivary IL-1β levels were elevated in naswar users as compared to controls.

Comparison of the Quality of Life of Patients with Mandibular Third Molar with Mild Pericoronitis Treated By Extraction or Periodontal Approach

Pericoronitis is an acute or chronic periodontal inflammatory condition usually affecting the mandibular third molars characterized by the infection of the mucosa covering semi-fully erupted tooth. The aim of the study is to evaluate and compare surgical and conservatively managed third molars with mild pericoronitis at first, third, and sixth months; we also aimed to rate quality of life of patients with Oral Health Impact Profile-14 (OHIP-14) index.

Removal of Pre-Existing Periodontal Inflammatory Condition before Tooth Extraction Ameliorates Medication-Related Osteonecrosis of the Jaw–Like Lesion in Mice

Medication-related osteonecrosis of the jaw (MRONJ) is a rare but detrimental intraoral lesion that predominantly occurs in patients with long-term use of antiresorptive agents, such as bisphosphonate and denosumab, a human anti-receptor activator of NF-κB ligand (RANKL) monoclonal antibody (Ab). Surgical intervention, such as tooth extraction, is a known risk factor for MRONJ, which is often performed to eliminate preexiting pathologic inflammatory conditions, such as periodontal diseases. Nonetheless, it remains unknown whether pre-existing periodontal disease condition exacerbates, or removal of such condition ameliorates, MRONJ development after tooth extraction. In this study, we combined the ligature-induced periodontitis and the tooth extraction mouse models under the administration of zoledronic acid (ZOL) or anti-RANKL Ab, and provide experimental evidence that a pre-existing pathologic inflammatory condition exacerbates MRONJ development after tooth extraction in mice. Under ZOL administration, tooth extraction alone induced ONJ lesions; however, extraction of a ligature-placed tooth further exacerbated ONJ development. When the ligature was removed and theinflammatory condition was deescalated, ONJ development was ameliorated. Anti-RANKL Ab administration resulted in similar outcomes. Interestingly, unlike ZOL-administered mice, anti-RANKL Ab-administered mice exhibited complete absence of osteoclasts, suggesting that physical presence of osteoclasts is not directly involved in ONJ development. Collectively, our study demonstrated that periodontal disease is a functionally linked risk factor that predisposes ONJ development after tooth extraction in the presence of bisphosphonate and denosumab.

Self-perceived oral symptoms and periodontal inflammatory conditions in habitual naswar dippers

Objectives:To compare self-perceived oral symptoms and clinical (plaque index [PI], bleeding on probing [BOP], clinical attachment loss [CAL]) and radiographic (marginal bone loss [MBL]) periodontal parameters among naswar (NW) and non-naswar dippers (NNW).Methods:One hundred and forty-two individuals (72 patients consuming naswar and 70 controls) were included. All participants completed a baseline questionnaire that included information regarding demographic characteristics and self-perceived oral symptoms. Clinical periodontal parameters (PI, BOP, PD and CAL) were recorded. MBL was measured on digital panoramic radiographs.Results:Pain in teeth, pain on chewing, bleeding gums and burning sensation in the mouth was significantly worse among NW than NNW (p<0.01). Clinical periodontal parameters and MBL were significantly high in NW than NNW (p<0.001). There was statistically significant influence of daily use and mean duration of naswar consumption on the severity of PI, BOP, PD (4 to 6 and >6 mm) and MBL among NW group.Conclusions:Self-perceived oral symptoms and periodontal parameters were worse among naswar dippers. It is highly recommended that naswar dipping should be considered a potential threat that could have major effects on periodontal tissues.

Is Periodontitis and Rheumatoid Arthritis Inter-Related?

There is a growing awareness of the link between periodontal and systemic inflammatory conditions, such as RA. Inflammation plays a key role in the origin of RA, its chronification, and in a progression of the disease with soft and hard tissue destruction, in a way similar to the situation seen in patients with chronic periodontitis. While the existing level of evidence is low, the association may be reflective of common underlying dysregulation of an inflammatory response in these individuals, and it seems that a decrease in periodontal inflammation in some way influences the level of systemic inflammation, and appears to contribute to the clinical improvement of the disease.

Estimation of salivary and serum alkaline phosphatase level as a diagnostic marker in type-2 diabetes mellitus with periodontal health and disease: A clinico-biochemical study.

Introduction:Chronic periodontitis is a multifactorial disease resulting in the inflammation and destruction of the supporting structures around the teeth, leading to tooth mobility and subsequent loss of tooth. Metabolic disorders, such as diabetes mellitus, play a crucial role in the progression of periodontal inflammatory conditions. Alkaline phosphatase (ALP) enzyme plays a key role in gingival inflammation and bone resorption. Hence, the aim of the present study is to compare the serum and salivary alkaline phosphatase levels in chronic periodontitis patients with or without type-2 diabetes mellitus.Materials and Methods:A total of 45 individuals were included in the study and divided into three groups: Group I (healthy individual), Group II (Chronic periodontitis without diabetes mellitus type-2) and Group III (Chronic periodontitis with type-2 diabetes mellitus) on the basis of clinical, radiographic and blood sugar examination. The serum and unstimulated saliva were collected from all patients in aseptic condition and samples were analyzed for alkaline phosphatase level using AVANTOR™ Benesphera ALP Kit by fully automated analyzer.Results:The result showed that the concentration of serum and salivary alkaline phosphatase increases significantly in patients with chronic periodontitis with type-2 diabetes mellitus than chronic periodontitis without diabetes mellitus and healthy patients.Conclusion:We can conclude that alkaline phosphatase can be used as a key inflammatory diagnostic biomarker in periodontal diseases.

Influence of interventional nonsurgical periodontal treatment on levels of salivary and serum nitric oxide in smokers and nonsmokers with chronic periodontitis.

Background and Objective:Nitric oxide (NO) is a widespread signaling molecule which is known to influence varied biological processes. However, an uncontrolled high level of NO accelerates tissue destruction. The pathogenesis of periodontal disease is also affected by smoking which alters the inflammatory response. The present study was thus performed to assess the effect of nonsurgical periodontal treatment on salivary and serum NO levels in smokers and nonsmokers with chronic periodontitis.Materials and Methods:Forty patients with chronic periodontitis, including 20 nonsmokers and equal number of smokers participated in the present study. Probing depth, clinical attachment level, plaque index, gingival index were assessed, serum and saliva samples were obtained from the patients at baseline and after Phase I therapy at 6 weeks to estimate NO by Griess colorimetric reaction.Results:Smokers showed higher serum and saliva NO levels 30.3 ± 3.28 and 50.4 ± 4.07 μM as compared to nonsmokers 20.05 ± 2.42 μM and 37.5 ± 2.95 μM, respectively, at baseline. After Phase I therapy, both the groups exhibited significant improvement in clinical parameters and reduction in serum and saliva NO levels; however, reduction was higher in nonsmokers.Conclusion:More destructive expression of periodontal disease in smokers causes an increase in the concentrations of NO and less reduction after Phase I therapy as compared to nonsmokers with chronic periodontitis. Hence, NO levels in saliva and serum could be used as indicators of periodontal inflammatory condition.

Periodontal treatment and HbA1c levels in subjects with diabetes mellitus.

It has earlier been reported that individuals with poorly controlled diabetes have severe periodontal disease (PD) compared to well-controlled diabetes. This longitudinal interventional study compared periodontal treatment outcomes with HbA1c level changes in four groups of diabetic and non-diabetic patients with or without PD, respectively. HbA1c, bleeding on probing (BOP), plaque index and periodontal pocket depth (PPD) 4 < 6 mm and ≥6 mm were recorded at baseline to 3 months after non-surgical treatment and 3-6 months for surgical treatment in subjects with or without T2D, and with or without PD. A total of 129 patients were followed from baseline to 6 months. Diabetics with PD and without PD showed reductions in HbA1c levels with a mean value of 0·3% after 3 months and mean values of 1% and 0·8%, respectively, after 6 months. Diabetics with PD showed higher levels of BOP versus non-diabetics without PD (P < 0·01) and versus diabetics without PD (P < 0·05) at baseline. After 6 months, diabetics with PD showed higher number of PPD 4 < 6 mm versus diabetics without PD (P < 0·01) and non-diabetics with PD (P < 0·01). Diabetics without PD showed higher levels of PPD 4 < 6 mm versus non-diabetics without PD (P < 0·01). Surgical and non-surgical periodontal treatment in all groups improved periodontal inflammatory conditions with a decrease in HbA1c levels in a period of three and 6 months. No change was seen in the number of pockets PPD 4 < 6 mm in diabetic subjects with PD after non-surgical and surgical treatment.

Comparison of periodontal inflammatory conditions among habitual gutka chewers and betel quid chewers.

The aim was to compare the periodontal inflammatory conditions among habitual gutka chewers and betel quid (BQ) chewers. Forty-five gutka chewers, 45 BQ chewers and 50 non-chewers (controls) were included. Demographic data regarding age, gender, duration, and frequency of gutka- and BQ-chewing habits and gingival bleeding were collected using a questionnaire. Clinical periodontal parameters [plaque index (PI), bleeding on probing (BOP), probing depth (PD) and clinical attachment loss (AL)] were recorded. Marginal bone loss (MBL) was measured on digital panoramic radiographs. Group differences in periodontal inflammatory parameters were tested using univariate and multivariable analyses (α < 5%). Periodontal inflammatory parameters [PI, BOP, PD (4-6 and >6 mm), clinical AL and MBL] were significantly high in gutka and BQ chewers than controls. There was no significant difference in periodontal inflammatory parameters among gutka and BQ chewers. The odds for gingival bleeding were six times and 13 times higher in gutka and BQ chewers, respectively, compared to controls. Comparison of gutka and BQ chewers did not significantly increase the odds of gingival bleeding. Periodontal inflammatory conditions were comparable among habitual gutka and BQ chewers; which suggests that gutka chewers and BQ chewers are equally susceptible to periodontal disease.

Periodontal Inflammatory Conditions Among Gutka Chewers and Non‐chewers With and Without Prediabetes

It is known that gutka chewing jeopardizes periodontal health; however, severity of periodontal inflammation in gutka chewers with and without prediabetes remains unknown. The aim of this study is to investigate the association of periodontal inflammatory conditions with gutka chewing and prediabetes. In this cross-sectional study, the effect of gutka use on periodontal health is investigated among 44 individuals with prediabetes and 44 without prediabetes. Demographic information regarding age, sex, duration of prediabetes, and gutka-chewing habits was collected using a questionnaire. Periodontal inflammatory conditions (plaque index [PI], bleeding on probing [BOP], probing depth [PD], marginal bone loss [MBL]) and fasting blood glucose levels (FBGLs) were recorded. Group differences in periodontal inflammatory parameters were tested using univariate and multivariable analyses (α ≤5%). Periodontal inflammatory parameters (PI, BOP, and PD) were significantly higher in individuals with prediabetes irrespective of gutka-chewing habit (P <0.05). Odds of periodontal inflammation in individuals with prediabetes were nine times higher than in healthy controls (95% confidence interval [CI] = 3.4 to 23.6). Gutka chewing alone, chewing among individuals with prediabetes, and chewing among healthy controls did not significantly increase the odds of periodontal inflammatory conditions. Individuals with prediabetes were significantly more likely to have periodontal inflammation than individuals without prediabetes even after controlling for sex and gutka chewing (odds ratio = 13.2; 95% CI = 4.3 to 40.7). In medically healthy individuals, periodontal inflammatory conditions are worse in gutka chewers compared to non-chewers; in patients with prediabetes, the severity of periodontal inflammation is governed by hyperglycemia when compared to habitual gutka usage.

Periodontal Disease in Habitual Cigarette Smokers and Nonsmokers With and Without Prediabetes

IntroductionPrediabetes and habitual cigarette smoking are significant risk factors contributing to periodontal disease. The aim was to assess the clinical and radiological markers of periodontal disease in habitual cigarette smokers and nonsmokers with and without prediabetes. MethodsSixty-eight individuals with prediabetes (test group; 34 smokers and 34 nonsmokers) and 68 medically healthy individuals (control group; 34 smokers and 34 nonsmokers) were included. Sociodemographic information, duration of smoking habit and number of cigarettes smoked daily were recorded through a questionnaire. Fasting blood glucose levels and periodontal inflammatory conditions (plaque index [PI], bleeding on probing [BOP] and probing pocket depth [PPD] of 4 to <6mm and ≥6mm) were recorded. In both groups, marginal bone loss (MBL) was measured on digital panoramic radiographs. ResultsCigarette smokers and nonsmokers in the test group had significantly higher fasting blood glucose level when compared with cigarette smokers in the control group (P<0.001). In the test group, there was no significant difference in PI, BOP, PPD (4 to <6mm and ≥6mm) and MBL among cigarette smokers and nonsmokers. Cigarette smokers in the control group had significantly higher PI (P<0.001), PPD (4 to <6mm; P<0.001), PPD ≥6mm (P<0.01) and MBL (P<0.05) than nonsmokers. BOP was significantly reduced in smokers when compared with nonsmokers in the control group (P<0.001). ConclusionsCigarette smokers without prediabetes exhibit significantly severe periodontal disease than nonsmokers. In subjects with prediabetes, the severity of periodontal disease seems to be over shadowed by the hyperglycemic state, obscuring the effect of habitual smoking.