Effect of Twinlight Laser on the Attachment of Human Gingival Fibroblasts to the Root Surface In Vitro.

BACKGROUND This study aimed to compare the effectiveness of subgingival scaling and root planing with the Twinlight laser, Er: YAG laser, and hand instrumentation on the removal of endotoxin and attachment of human gingival fibroblasts (HGFs) to cementum surfaces in vitro. MATERIAL AND METHODS Single-rooted teeth extracted for periodontal disease were collected and divided into 3 groups: group A, root planing with Gracey curet no. 5/6; group B, irradiation with Er: YAG laser; group C, irradiation with Er: YAG laser and Nd: YAG laser. Endotoxins were determined by the limulus amebocyte lysate test. Cell attachment and proliferation of HGFs on root specimens were evaluated by cell counting kit-8 assay. The root surface and cell morphology were observed by scanning electron microscope. RESULTS A flat root surface with scratches was found in group A, Group B had a homogeneous rough morphology without carbonization, and group C had a non-homogeneous rough morphology with ablation. The endotoxin concentration was highest in group A (P<0.05) and lowest in group C (P>0.05). HGFs cultured in group B showed significantly increased adhesion and proliferation compared with groups A and C (P<0.05). HGFs in group B were well attached, covered densely by pseudopodia. HGFs in group A were round with poor extension and short pseudopodia, while the cells in the group C were in narrow, triangular, or polygonal shapes. CONCLUSIONS Twinlight laser-assisted periodontal treatment effectively improved the biocompatibility of root surface and promoted the attachment and proliferation of fibroblasts by removing calculus and reducing the concentration of endotoxins.

Saliva pH and Flow Rate in Patients with Periodontal Disease and Associated Cardiovascular Disease.

BACKGROUND Periodontal disease, a frequent oral health problem, is connected with cardiovascular morbidity and mortality. This study aimed to assess the unstimulated saliva flow rate and saliva pH as markers of the severity of periodontal disease in patients with cardiovascular disease. MATERIAL AND METHODS A cohort of 155 patients (78 men and 77 women, aged 30-92 years) was included, and a structured questionnaire obtained information about their health status, oral healthcare behaviors, and eating habits. An oral examination was performed to assess periodontal status and presence of dental calculus. The unstimulated whole salivary flow rate and salivary pH were measured. An oral hygienization was performed, and 3 months later, salivary flow rate and pH were reevaluated. RESULTS A severe form of periodontal disease was found in 22.4% of patients. Disease severity was strongly correlated with low pH values (6.25 in stage IV periodontal disease), lower salivary flow rate (0.28 mL/min), smoking, poor oral hygiene habits and obesity, with no significant differences by sex. We observed a significant increase of pH (up to 6.30±0.17) in patients with severe periodontal disease (P=0.001) and salivary flow rate values (0.29±0.07 mL/min; P=0.014) 3 months after oral hygienization. There was a strong association between the severity of periodontal disease and presence of cardiovascular disease (P=0.001). CONCLUSIONS Our study suggests that the decrease of salivary flow rate and pH level might be associated with the severity of periodontal disease.

Experimental Periodontal Disease Triggers Coronary Endothelial Dysfunction in Middle-Aged Rats: Preventive Effect of a Prebiotic ß-Glucan.

This study was aimed to verify the hypothesis that periodontal disease contributes to endothelial dysfunction in the coronary arteries of middle-aged rats. Besides we evaluated the effects of a prebiotic (ß-glucan isolated from Saccharomyces cerevisiae) in preventing vascular dysfunction. The sample comprised young (sham and induced to periodontal disease) and middle-aged rats (sham, periodontal disease, sham-treated and periodontal disease-treated), at 12 and 57 weeks, respectively. The treated-groups received daily doses of ß-glucan (50 mg/kg) orally (gavage) for 4 weeks, and periodontal disease was induced in the last 2 weeks by ligature. A myograph system assessed vascular reactivity. The expression of endothelial nitric oxide synthase (eNOS), cyclooxygenase 1 (COX-1), COX-2, p47phox, gp91phox, NF-KB p65, p53, p21, and p16 was quantified by western blotting. Serum hydroperoxide production was measured by the ferrous oxidation-xylenol orange (FOX-2) assay method. Interleukin-1 beta (IL-1ß), IL-10, and tumor necrosis factor-alpha (TNF-α) levels were evaluated by spectroscopic ultraviolet-visible analysis. Periodontal disease in middle-aged rats was associated with reduced acetylcholine-induced relaxations of coronary artery rings affecting the endothelium-dependent hyperpolarization- and the nitric oxide-mediated relaxations. The endothelial dysfunction was related to eNOS downregulation, pronounced impairment of the EDH-mediated relaxation, increased IL-1ß and TNF-α proinflammatory cytokines, and also upregulation of NADPH oxidase and COXs, starting accumulate aging markers such as p53/p21 and the p16. Treatment with ß-glucan effectively reduced bone loss in periodontal disease and delayed endothelial dysfunction in the coronary artery. Our data show that yeast ß-glucan ingestion prevented oxidative stress and synthesis of proinflammatory marker and prevented eNOS reduction induced by periodontal disease in middle-aged rats. These results suggest that ß-glucan has a beneficial effect on the coronary vascular bed.

The Association Between Periodontal Disease and Breast Cancer in a Prospective Cohort Study.

Periodontal disease may be associated with increased breast cancer risk, but studies have not considered invasive breast cancer and ductal carcinoma in situ (DCIS) separately in the same population. We assessed the relationship between periodontal disease and breast cancer in a large prospective cohort study. The Sister Study followed women without prior breast cancer ages 35 to 74 years from 2003 to 2017 (N = 49,968). Baseline periodontal disease was self-reported, and incident breast cancer was ascertained over a mean follow-up of 9.3 years. We estimated hazard ratios (HR) and 95% confidence intervals (CI) using Cox proportional hazards regression, adjusting for multiple potential confounders, including smoking status. Heterogeneity in risk for invasive breast cancer versus DCIS was also estimated. About 22% of participants reported a history of periodontal disease at baseline. A total of 3,339 incident breast cancers (2,607 invasive breast cancer, 732 DCIS) were identified. There was no clear association between periodontal disease and overall breast cancer risk (HR = 1.02; 95% CI, 0.94-1.11). However, we observed a nonstatistically significant suggestive increased risk of invasive breast cancer (HR = 1.07; 95% CI, 0.97-1.17) and decreased risk of DCIS (HR = 0.86; 95% CI, 0.72-1.04) associated with periodontal disease, with evidence for heterogeneity in the risk associations (relative HR for invasive breast cancer versus DCIS = 1.24; 95% CI, 1.01-1.52). A case-only analysis for etiologic heterogeneity confirmed this difference. We observed no clear association between periodontal disease and overall breast cancer risk. The heterogeneity in risk associations for invasive breast cancer versus DCIS warrants further exploration.

Periodontal clinico-morphological changes in patients wearing old nickel-chromium and copper alloys bridges.

Elderly population frequently presents more than one prosthetic restoration realized from different types of dental alloys which, in time, suffer various alterations in the oral environment. Metallic ions are released in saliva due to its electrolytic qualities, interacting with the contact tissues. Studies regarding cytotoxicity of dental alloys are providing contradictory results. Besides biocompatibility, the microbial factor is also greatly influencing the long-term success of the prosthetic rehabilitation. This study's aim was to assess the response of the gingival tissue to nickel-chromium (Ni-Cr) and copper (Cu)-based dental casting alloys from fixed dentures present in many patients from Romania. Gingival samples were taken from 124 patients wearing fixed dental restorations made from these two types of alloys from injured areas surrounding the abutment teeth; histological specimens were prepared, fixed in 10% neutral buffered formalin, paraffin-embedded and stained with Hematoxylin-Eosin (HE). Histological analysis showed the existence of a chronic inflammatory infiltrate in the gingival chorion, necrosis areas, and vascular congestion. Various morphological alterations appeared, depending on the intensity of the inflammation and the immune response. The surface epithelium suffered a hyperplasic reaction, either limited to acanthosis or involving the whole epithelium, the release of the Cu(2+) and Ni(2+) ions from the dental alloys used in bridges and crowns being responsible for inducing gingival hyperplasia and a chronic inflammation in the areas situated around the abutment teeth. The immunohistochemical study allowed us to observe an increased number of positive cluster of differentiation 3 (CD3) T-lymphocytes in periodontium, proving that the cellular immune response is rapid and intense.

Pivotal Role of Tenascin-W (-N) in Postnatal Incisor Growth and Periodontal Ligament Remodeling.

The continuously growing mouse incisor provides a fascinating model for studying stem cell regulation and organ renewal. In the incisor, epithelial and mesenchymal stem cells assure lifelong tooth growth. The epithelial stem cells reside in a niche known as the cervical loop. Mesenchymal stem cells are located in the nearby apical neurovascular bundle and in the neural plexus. So far, little is known about extracellular cues that are controlling incisor stem cell renewal and guidance. The extracellular matrix protein tenascin-W, also known as tenascin-N (TNN), is expressed in the mesenchyme of the pulp and of the periodontal ligament of the incisor, and is closely associated with collagen 3 fibers. Here, we report for the first time the phenotype of tenascin-W/TNN deficient mice, which in a C57BL/6N background exhibit a reduced body weight and lifespan. We found major defects in the alveolar bone and periodontal ligament of the growing rodent incisors, whereas molars were not affected. The alveolar bone around the incisor was replaced by a dense scar-like connective tissue, enriched with newly formed nerve fibers likely leading to periodontal pain, less food intake and reduced body weight. Using soft food to reduce mechanical load on the incisor partially rescued the phenotype. In situ hybridization and Gli1 reporter mouse experiments revealed decreased hedgehog signaling in the incisor mesenchymal stem cell compartment, which coordinates the development of mesenchymal stem cell niche. These results indicate that TNN deficiency in mice affects periodontal remodeling and increases nerve fiber branching. Through periodontal pain the food intake is reduced and the incisor renewal and the neurovascular sonic hedgehog secretion rate are reduced. In conclusion, tenascin-W/TNN seems to have a primary function in rapid periodontal tissue remodeling and a secondary function in mechanosensation.

RNA sequencing for ligature induced periodontitis in mice revealed important role of S100A8 and S100A9 for periodontal destruction.

Periodontitis is an inflammatory disease caused by pathogenic oral microorganisms that induce the destruction of periodontal tissue. We sought to identify the relevant differentially expressed genes (DEGs) and clarify the mechanism underlying the rapid alveolar bone loss by using ligature-induced periodontitis in mice. A silk ligature was tied around the maxillary left second molar in 9-week-old C57BL/6 J male mice. In-vivo micro-CT analysis revealed that ligation induced severe bone loss. RNA-sequencing analysis, to examine host responses at 3 days post-ligation, detected 12,853 genes with fragments per kilobase of exon per million mapped reads ≥ 1, and 78 DEGs. Gene ontology term enrichment analysis revealed the expression profiles related to neutrophil chemotaxis and inflammatory responses were significantly enriched in the ligated gingiva. The expression levels of innate immune response-related genes, including S100a8 and S100a9, were significantly higher in the ligated side. S100A8 was strongly detected by immunohistochemistry at the attached epithelium in ligated sites. Inhibition of S100A8 and S100A9 expression revealed that they regulated IL1B and CTSK expression in Ca9-22 cells. Thus, innate immune response-related molecules might be associated with the burst-destruction of periodontal tissue in ligature-induced periodontitis. Especially, S100A8 and S100A9 may play an important role in alveolar bone resorption.

Identification of Aberrantly Expressed lncRNAs Involved in Orthodontic Force Using a Subpathway Strategy.

BACKGROUND: The aim of the study was to identify key long noncoding RNAs (lncRNA) and related subpathways in the periodontal ligament tissue following orthodontic force. METHODS: We adopt a novelty subpathway strategy to identify lncRNAs competitively regulated functions and the key competitive lncRNAs in periodontal ligament disorders after undergoing orthodontic force. To begin with, patients with orthodontics in our hospital were enrolled in our research. The relationship of lncRNA-mRNA was established through shared predicted miRNA by using the hypergeometric test, Jaccard coefficient standardization, and the Pearson coefficient to determine the valid interaction relationship. After embedding screened lncRNA interactions to pathways, the significant subpathways were recognized by lenient distance and Wallenius approximation methods to calculate the false discovery rate value of each subpathway. RESULTS: The lncRNA-mRNA intersections including 263 lncRNAs, 1,599 mRNAs, and 3,762 interacting pairs were obtained. The enriched mRNAs were further enriched into various candidate pathways such as the PI3K-Akt signaling pathway. Several subpathways were screened, including the PI3K-Akt signaling pathway, 04510_1 focal adhesion, and p53 signaling pathway, respectively. The network of pathway-lncRNA-mRNA was constructed. Several key lncRNAs including DNAJC3-AS1, WDFY3-AS2, LINC00482, and DLEU2 were screened. CONCLUSIONS: DNAJC3-AS1, WDFY3-AS2, LINC00482, and DLEU2 as aberrantly expressed lncRNAs involved in orthodontic force might play crucial roles in periodontal ligament disease pathogenesis.

Gingival epithelial barrier: regulation by beneficial and harmful microbes.

The gingival epithelium acts as a physical barrier to separate the biofilm from the gingival tissue, providing the first line of defense against bacterial invasion in periodontal disease. Disruption of the gingival epithelial barrier, and the subsequent penetration of exogenous pathogens into the host tissues, triggers an inflammatory response, establishing chronic infection. Currently, more than 700 different bacterial species have been identified in the oral cavity, some of which are known to be periodontopathic. These bacteria contribute to epithelial barrier dysfunction in the gingiva by producing several virulence factors. However, some bacteria in the oral cavity appear to be beneficial, helping gingival epithelial cells maintain their integrity and barrier function. This review aims to discuss current findings regarding microorganism interactions and epithelial barrier function in the oral cavity, with reference to investigations in the gut, where this interaction has been extensively studied.

Dental abnormalities in individuals with pathogenic germline variation in DICER1.

Pathogenic germline variation in the microRNA processing gene DICER1 gives rise to an autosomal dominant, tumor-predisposition disorder. Conditional deletion of Dicer1 in murine dental epithelium shows that it controls tooth patterning, size, number, and shape. The human dental phenotype of people with germline pathogenic variation in DICER1 is unknown. DICER1-carriers (n = 57) and family controls (n = 55) were evaluated at the NIH Clinical Center dental clinic as part of a comprehensive medical evaluation. Digital panoramic radiographs, bite-wing radiographs, and oral photographs were collected. A single observer, blind to DICER1 status, reviewed the dental records and determined the presence or absence of 11 dental characteristics as described in the clinic notes, radiographs, or oral photographs. Subjective phenotypes were reviewed on radiographs by two examiners (blind to DICER1 status) for the presence or absence of the dental characteristics to reduce inconsistencies. By simple association, bulbous crown, periodontitis, and taurodontism were all significant (p < .05). Logistic regression with chi-square maximum likelihood estimates showed that bulbous crown and periodontitis remained significant. Recognition of these phenotypes may aid identification of individuals and families at risk for DICER1-associated neoplasms. These findings may also guide dental care for individuals with germline DICER1 pathogenic variation.

Association of periodontal disease with depression and adverse birth outcomes: Results from the Perinatal database; Finger Lakes region, New York State.

Preterm and low birth weight infants are at greater risk for mortality and a variety of health and developmental problems. Data from the Finger Lakes Perinatal Data System database on 316,956 deliveries occurring between 2004-2014 and pregnancy outcomes were analyzed to assess the association of periodontal (gum) disease with depression, other maternal factors and adverse birth outcomes. Adjusted effects of periodontal disease and depression on adverse birth outcomes were estimated using multiple logistic regression models and path analysis. Having preterm delivery was associated significantly with depression (OR = 1.177; 95% CI: [1.146, 1.208]), having adequate health care (OR = 1.638; 95% CI: [1.589, 1.689]), smoking during pregnancy (OR = 1.259; 95% CI: [1.220, 1.300]), and being less educated (OR = 1.214; 95% CI: [1.174, 1.256]). Having low birth weight was significantly associated with depression (OR = 1.206; 95% CI: [1.170, 1.208]), smoking during pregnancy (OR = 1.855; 95% CI: [1.793, 1.919]), and being less educated (OR = 1.322; 95% CI: [1.275, 1.370]). Periodontal disease was significantly associated with alcohol use during pregnancy (OR = 1.314; 95% CI: [1.227, 1.407]) and white race (OR = 1.192; 95% CI: [1.167, 1.217]). Depression was significantly associated with periodontal disease (OR = 1.762; 95% CI: [1.727, 1.797]) and alcohol use during pregnancy (OR = 1.470; 95% CI: [1.377, 1.570]). We concluded that a positive association existed between depression during pregnancy and adverse birth outcomes, and that depression served as a mediator in the association of periodontal disease with adverse birth outcomes.

Berberine promotes osteogenic differentiation of mesenchymal stem cells with therapeutic potential in periodontal regeneration.

Periodontal disease is a bacterial infection-associated disease of the periodontal tissues characterized by the destruction of tooth-supporting structures, including alveolar bone. The ideal goal of periodontal therapy is the complete regeneration of alveolar bone in a healthy microenvironment free of infection. In this study, we found that berberine, a benzylisoquinoline plant alkaloid from Coptidis Rhizoma, strongly inhibited the growth of Porphyromonas gingivalis. Gingipain is the most important virulence factor of Porphyromonas gingivalis in the process of periodontal tissue destruction. Berberine also had an inhibitory effect on gingipain activity in a concentration dependent manner. Remarkably, berberine restored the downregulation of osteogenesis-related genes expression in bone mesenchymal stem cells (BMSCs) induced by Porphyromonas gingivalis infection, and significantly increased the expression of osteogenesis-related genes such as OSX, COLI, ALP, OCN and OPN compared to the control group. This results suggested that berberine may directly promote osteogenesis. Further in-vitro studies demonstrated that berberine statistically significantly promoted the osteogenic differentiation of BMSCs at concentrations of 1-10 µM. In the research on the mechanisms, we found that both total ß-catenin and nuclear ß-catenin accumulation were statistically significantly increased by berberine. And the transcriptional activity of ß-catenin/TCF was about 2 folds higher than the control group. Furthermore, Wnt signalling specific inhibitor DKK-1 blocked the above effects of berberine. These demonstrated that Wnt/ß-catenin signalling pathway was involved in the osteogenic differentiation induced by berberine. The antibacterial actions in combination with the promotion role in osteogenic differentiation position berberine as a prospective drug for periodontal tissue regeneration.

Understanding the pathophysiology behind chairside diagnostics and genetic testing for IL-1 and IL-6.

In order for chairside diagnostic testing to make an impact on dental therapy, practitioners require a better understanding of genetic mutations contributing to the pathophysiology of periodontal disease. Commensal and pathogenic bacterial colonization in oral cavity tissues produces a cascade of proinflammatory signaling pathways ultimately detrimental to host tissues. Resolving inflammation is a multifactorial process involving the downregulation of proinflammatory cytokines while allowing commensal bacterial levels to return to normal. Because of the complicated nature of commensal bacteria and oral health homeostasis, the emphasis of dental therapy should place renewed focus on limiting destructive inflammation rather than solely eliminating bacteria. Salivary diagnostics are an easy, non-invasive way to assess inflammatory markers. Inflammatory cytokine levels can help determine the subclinical health of a patient, showing the transition from health to gingivitis, or periodontitis, prior to clinical presentation. Single nucleotide polymorphism mutations can aid in determining increased risk of developing periodontitis. Taken together, and alongside regular clinical evaluations, chairside diagnostics help individualize treatment plans to slow, or halt, the progression of disease-before tissue destruction can take place. While more studies are needed analyzing specific mutations across periodontal categories, chairside diagnostics present an exciting adjunct to improve patient care.

Melatonin promotes reduction in TNF levels and improves the lipid profile and insulin sensitivity in pinealectomized rats with periodontal disease.

AIM: This study aimed to investigate the effects of melatonin (ME) on insulin resistance (IR) and signaling (IS), proinflammatory cytokine levels, and lipid profiles in pinealectomyzed (PNX) rats with periodontal disease (PD). MAIN METHODS: One hundred and forty-four rats (age = 40 days) were distributed into 8 groups: 1) control (CN); 2) PD only; 3) PNX only; 4) PNX and PD (PNXPD); 5) CN treated with ME (CNM); 6) PD treated with ME (PDM); 7) PNX treated with ME(PNXM); 8) PNX and PD treated with ME(PNXPDM). The PNX groups were subjected to pinealectomy at 40 and at 60 days of age. The animals were then subjected to PD induction in the mandibular first molars. After PD induction, the ME replacement therapy (MERT-5 mg/kg body weight) was performed using water for 28 days. After this period, the plasma concentration of glucose, insulin, TNF, IL-6, triglycerides, total cholesterol, HDL-cholesterol, LDL-cholesterol, and VLDL-cholesterol and the HOMA-IR index were determined. Akt serine phosphorylation status in the white adipose tissue, gastrocnemius muscle, and rat liver were also evaluated. KEY FINDINGS: PD, PNX, and PNXPD groups showed an increase in IR with elevated plasma levels of insulin and TNF compared to CN group. PNX and PNXPD groups presented alteration in lipid profile compared to CN group. MERT improved all of the analyzed parameters. No difference was observed in the IS among different groups. SIGNIFICANCE: The results suggest that MERT efficiently prevents IR, improves lipid profile, and increases plasma levels of insulin and TNF in PD and PNX rats.

Protective effects of metformin, statins and anti-inflammatory drugs on head and neck cancer: A systematic review.

The main objective of this study was to evaluate the effect of metformin, statins and anti-inflammatory drugs (NSAIDs) on head and neck cancer (HNC). Specifically, the potential beneficial effects on risk, survival and recurrence based on epidemiological studies. PRISMA guidelines were followed. After searching MEDLINE (PubMed), IBECS, LILACS and the Cochrane Central Register for Controlled Trials, 13 studies met the inclusion criteria and so underwent qualitative synthesis (six studies for metformin and seven for NSAIDs). No studies were found for statins. Studies varied in their methodological quality. Meta-analyses showed that metformin exerts significant beneficial effects on HNC risk (RR = 0.71 95% CI 0.61-0.84) and overall survival (RR = 1.71 95% CI 1.20-2.42). Qualitative synthesis also suggests an apparently dose-response relationship and increased benefit when administered alone. The pooled-analyses yielded an almost significant effect of NSAIDs on HNC risk (RR = 0.86 95% CI 0.74-1.01). No associations were found between aspirin use and the risk of HNC (RR = 0.98 95% CI 0.77-1.24) and overall survival (RR = 1.10 95% CI 0.89-1.36). Metformin appears to have beneficial effects on HNC risk and overall survival, with an apparently dose-response relationship and increased benefit when administered alone. NSAIDs also seem to have a modest beneficial effect on HNC risk. No definitive conclusions can be reached for aspirin as the evidence available was proved inconsistent. Further research by means of well designed and conducted studies are needed to determine firm clinical implications. Standardized assessment methods for HNC outcomes should be established and account for known confounding factors such as smoking and alcohol consumption.

Retrieval of a periodontally compromised tooth by allogeneic grafting of mesenchymal stem cells from dental pulp: A case report.

Objective To report a case of successful allogeneic grafting of mesenchymal dental pulp stem cells (DPSCs) as preliminary findings in a patient with periodontal disease enrolled into clinical trial ISRCTN12831118. Methods Mesenchymal stem cells from the dental pulp of a deciduous tooth from a 7-year-old donor were separated from the pulp chamber and processed via enzymatic digestion and centrifugation. DPSCs were passaged and cultured on a 35 × 13 mm culture dish in minimum essential medium-alpha, without supplementation. After reaching 80% confluency, 5 x 106 allogeneic DPSCs in 250 µl phosphate buffered saline were seeded onto a dry scaffold of lyophilized collagen-polyvinylpyrrolidone sponge placed in the left lower premolar area of a 61-year-old patient with periodontal disease. Surgical access to the lower premolar area was achieved using the flap technique. Results At 3 and 6 months following allogeneic graft, the patient showed no sign of rejection and exhibited decreases in tooth mobility, periodontal pocket depth and bone defect area. Bone mineral density had increased at the graft site. Conclusions Regenerative periodontal therapy using DPSCs of allogeneic origin may be a promising treatment for periodontal disease-induced bone defects.

Periodontal health status and lung function in two Norwegian cohorts.

RATIONALE AND OBJECTIVES: The oral cavity is united with the airways, and thus poor oral health may affect respiratory health. However, data on the interaction of periodontal and respiratory health is limited. We aimed to evaluate whether periodontal health status, assessed by the Community Periodontal Index (CPI), was related to lung function among young and middle-aged adults in two Norwegian cohorts. METHODS: Periodontal health status and lung function were measured among 656 participants in the Norwegian part of the European Community Respiratory Health Survey (ECHRS III) and the RHINESSA offspring study. Each participant was given a CPI-index from 0 to 4 where higher values reflect poorer periodontal status. The association between CPI and lung function was estimated with linear regression adjusting for age, gender, smoking, body mass index, exercise, education, use of antibiotics, inhaled medication and corrected for clustering within families. MAIN RESULTS: Participants with CPI 3-4 had significantly lower FEV1/FVC ratio compared to participants with CPI 0, b (95% CI) = -0.032 (-0.055, -0.009). Poorer periodontal health was associated with a significant decrease in the FEV1/FVC ratio with an adjusted regression coefficient for linear trend b (95% CI) = -0.009 (-0.015, -0.004) per unit increase in CPI. This negative association remained when excluding asthmatics and smokers (-0.014 (-0.022, -0,006)). CONCLUSIONS: Poorer periodontal health was associated with increasing airways obstruction in a relatively young, healthy population. The oral cavity is united with the airways and our findings indicate an opportunity to influence respiratory health by improving oral health.

Periodontal parameters in prediabetes, type 2 diabetes mellitus, and non-diabetic patients

Abstract The aim of the present study was to compare the clinical and radiographic periodontal parameters in prediabetes, type 2 diabetes mellitus (T2DM), and non-diabetic patients. Forty-one patients with prediabetes (Group 1), 43 patients with T2DM (Group 2), and 41 controls (Group 3) were included. Demographic data were recorded using a questionnaire. Full-mouth clinical (plaque index [PI], bleeding on probing [BOP], probing depth [PD], clinical attachment loss [CAL], missing teeth [MT]) and radiographic (marginal bone loss [MBL]) parameters were measured on digital radiographs. In all groups, hemoglobin A1c (HbA1c) levels were also measured. P values less than 0.05 were considered statistically significant. The mean age and HbA1c levels of participants in Groups 1, 2, and 3 were 53.4±3.5, 60.1 ± 0.6, and 56.6 ± 2.5 years and 6.1%, 8.4%, and 4.8%, respectively. The mean duration of prediabetes and T2DM in patients from Groups 1 and 2 were 1.9 ± 0.3 and 3.1 ± 0.5 years, respectively. PI, BOP, PD, MT, CAL, and MBL were significantly higher in Groups 1 (p < 0.05) and 2 (p < 0.05) than in Group 3. There was no statistically significant difference in these parameters in Groups 1 and 2. Periodontal parameters were worse between prediabetes and T2DM patients compared with controls; however, these parameters were comparable between prediabetes and T2DM patients.

Periodontal diseases.

Periodontal diseases comprise a wide range of inflammatory conditions that affect the supporting structures of the teeth (the gingiva, bone and periodontal ligament), which could lead to tooth loss and contribute to systemic inflammation. Chronic periodontitis predominantly affects adults, but aggressive periodontitis may occasionally occur in children. Periodontal disease initiation and propagation is through a dysbiosis of the commensal oral microbiota (dental plaque), which then interacts with the immune defences of the host, leading to inflammation and disease. This pathophysiological situation persists through bouts of activity and quiescence, until the affected tooth is extracted or the microbial biofilm is therapeutically removed and the inflammation subsides. The severity of the periodontal disease depends on environmental and host risk factors, both modifiable (for example, smoking) and non-modifiable (for example, genetic susceptibility). Prevention is achieved with daily self-performed oral hygiene and professional removal of the microbial biofilm on a quarterly or bi-annual basis. New treatment modalities that are actively explored include antimicrobial therapy, host modulation therapy, laser therapy and tissue engineering for tissue repair and regeneration.

Post-Surgical Clinical Monitoring of Soft Tissue Wound Healing in Periodontal and Implant Surgery.

Clinical features of surgical soft tissue wound healing in dentistry have been rarely discussed in the international literature. The aim of the present paper is to highlight both the main clinical findings of surgical wound healing, especially in periodontal and implant dentistry, and the wound healing monitoring procedures which should be followed. Wound inspection after careful food and plaque debridement is the essential part of wound healing monitoring. Periodontal and peri-implant probing should be performed only after tissue healing has been completed and not on a weekly basis in peri-implant tissue monitoring. Telephone follow-up and patient self-assessment scales can also be used the days following surgery to monitor the most common surgical complications such as pain, swelling, bleeding, and bruising. Wound healing monitoring is an important concern in all surgical procedures since it allows to identify signs or/and symptoms possibly related to surgical complications.