Postmenopausal women with HIV have increased tooth loss.

BACKGROUND: With effective antiretroviral therapy, people with HIV (PWH) are living longer and aging; the majority of PWH in the United States are now over the age of 50 and in women have gone through the menopause transition. Menopause potentiates skeletal bone loss at the spine, hip, and radius in PWH. The alveolar bone which surronds the teeth is different than long bones because it is derived from the neural crest. However, few studies have assessed the oral health and alveolar bone in middle aged and older women with HIV. Therefore, the objective of this study was to evaluate periodontal disease and alveolar bone microarchitecture in postmenopausal women with HIV. METHODS: 135 self-reported postmenopausal women were recruited (59 HIV-, 76 HIV + on combination antiretroviral therapy with virological suppression) from a single academic center. The following parameters were measured: cytokine levels (IFN-γ, TNF-α, IL-1ß, IL-2, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, IL-17 A, OPG, and RANKL) in gingival crevicular fluid, bleeding on probing, probing depth, clinical attachment loss, number of teeth present, alveolar crestal height, and alveolar bone microarchitecture. RESULTS: The mean age of participants was 57.04+/-6.25 years and a greater proportion of women with HIV were black/African American (HIV + 68.42%, HIV- 23.73%; p < 0.001). There was no significant difference in bleeding on probing (p = 0.17) and attachment loss (p = 0.39) between women who were HIV infected vs. HIV uninfected. Women with HIV had significantly higher RANKL expression in Gingival Crevicular Fluid (HIV + 3.80+/-3.19 pg/ul, HIV- 1.29+/-2.14 pg/ul ; p < 0.001), fewer teeth present (HIV + 17.75+/-7.62, HIV- 22.79+/-5.70; p < 0.001), ), lower trabecular number (HIV + 0.08+/-0.01, HIV- 0.09+/-0.02; p = 0.004) and greater trabecular separation (HIV + 9.23+/-3.11, HIV- 7.99+/-3.23; p = 0.04) compared to women without HIV that remained significant in multivariate logistic regression analysis in a sub-cohort after adjusting for age, race/ethnicity, smoking status, and diabetes. CONCLUSION: Postmenopausal women with HIV have deterioration of the alveolar trabecular bone microarchitecture that may contribute to greater tooth loss.

Decoding the role of macrophages in periodontitis and type 2 diabetes using single-cell RNA-sequencing.

Macrophages are resident myeloid cells in the gingival tissue which control homeostasis and play a pivotal role in orchestrating the immune response in periodontitis. Cell heterogeneity and functional phenotypes of macrophage subpopulations in periodontitis remain elusive. Here, we isolated gingival tissue from periodontitis-affected and healthy sites of patients with and without type 2 diabetes mellitus (T2DM). We then used single-cell RNA-sequencing (scRNA-seq) to define the heterogeneity of tissue-resident macrophages in gingival tissue in health vs. periodontitis. scRNA-seq demonstrated an unforeseen gene expression heterogeneity among macrophages in periodontitis and showed transcriptional and signaling heterogeneity of identified subsets in an independent cohort of patients with periodontitis and T2DM. Our bioinformatic inferences indicated divergent expression profiles in macrophages driven by transcriptional regulators CIITA, RELA, RFX5, and RUNX2. Macrophages in periodontitis expressed both pro-inflammatory and anti-inflammatory markers and their polarization was not mutually exclusive. The majority of macrophages in periodontitis expressed the monocyte lineage marker CD14, indicating their bone marrow lineage. We also found high expression and activation of RELA, a subunit of the NF-κB transcription factor complex, in gingival macrophages of periodontitis patients with T2DM. Our data suggested that heterogeneity and hyperinflammatory activation of macrophages may be relevant to the pathogenesis and outcomes of periodontitis, and may be further augmented in patients with T2DM.

The impact of smoking on non-surgical periodontal therapy: A systematic review and meta-analysis.

AIM: Smoking is a risk factor for periodontitis. This study aimed to evaluate the impact of smoking on clinical outcomes of non-surgical periodontal therapy. MATERIALS AND METHODS: Electronic databases were searched to screen studies published before May 2020. The included studies had to have two groups: smokers (S) and non-smokers (NS) with periodontitis. The outcomes evaluated were differences between groups in probing depth (PD) reduction and clinical attachment level (CAL) gain after non-surgical periodontal therapy. Meta-regressions were conducted to evaluate correlations between outcomes and other contributing factors. RESULTS: Seventeen studies were included. The post-treatment PD reduction in the S group was smaller than in the NS group (weighted mean difference in PD reduction: -0.33 mm, 95% confidence interval (CI): [-0.49, -0.17], p < .01). The CAL gain in the S group was also smaller than in the NS group (weighted mean difference in CAL gain: -0.20 mm, CI: [-0.39, -0.02], p < .01). Additionally, baseline PD significantly affected the difference in PD reduction between two groups. CONCLUSIONS: Smoking negatively impacts clinical responses to non-surgical periodontal therapy. Smokers with periodontitis have significantly less PD reduction and CAL gain than non-smokers.

Immediate versus delayed temporization at posterior single implant sites: A randomized controlled trial.

AIMS: We conducted a randomized controlled trial to assess the clinical outcomes of two loading protocols involving either immediate or delayed prosthetic temporization of single implants placed at posterior, healed sites. MATERIALS AND METHODS: Forty-nine patients in need of single implants at premolar or molar sites were randomized to receive a temporary crown either immediately after implant placement or 3 months later. Randomization was stratified by sex, implant location (premolar/molar) and arch (maxilla/mandible). Final implant screw-retained zirconia crowns with angulated screw channels were delivered at 5 months after surgery. Radiographic bone levels (primary outcome), peri-implant mucosal margin levels and peri-implant probing depths were recorded at baseline, 6 and 12 months after surgery. RESULTS: Both treatment arms showed similar patterns of soft tissue and bone re-modelling from the implant platform over 12 months [mean bone level change 1.6 mm (SD 1.0 mm) in the delayed, and 1.2 mm (SD 1.3 mm) in the immediate temporization group], with the majority of changes occurring within the first 6 months. CONCLUSIONS: Immediate or delayed temporization of single implants placed at posterior healed sites resulted in largely similar 1-year outcomes with respect to peri-implant bone levels and soft tissue changes.

Impact of diabetes on clinical periodontal outcomes following non-surgical periodontal therapy.

AIM: This systematic review aimed to evaluate the impact of diabetes mellitus on clinical outcomes of non-surgical periodontal therapy. MATERIALS AND METHODS: Searches were conducted in electronic databases to screen studies published from January 1960 to August 2018. The included studies had at least two groups of patients: chronic periodontitis only (P) or both diabetes and chronic periodontitis (DMP). Outcomes of interest included the difference between the two groups in probing depth (PD) reduction and clinical attachment level (CAL) gain following non-surgical periodontal therapy. Meta-regression was conducted to evaluate the correlation between the outcomes of interest and contributing factors. RESULTS: A total of 12 studies with a follow-up period up to 6 months were included. There was no significant difference in PD reduction (p = 0.55) or CAL gain (p = 0.65) between the two groups. A positive association between PD reduction and baseline PD difference (p = 0.03), and a negative association between PD reduction and age (p = 0.04) were found. The level of HbA1c at baseline did not significantly affect the difference in PD reduction (p = 0.39) or CAL gain (p = 0.44) between two groups. CONCLUSIONS: Recognizing the study's limitations, we conclude that diabetes mellitus (HbA1c ≤ 8.5%) does not appear to significantly affect short-term clinical periodontal outcomes of non-surgical periodontal treatment.

Periodontal manifestations of systemic diseases and developmental and acquired conditions: Consensus report of workgroup 3 of the 2017 World Workshop on the Classification of Periodontal and Peri-Implant Diseases and Conditions.

BACKGROUND: A variety of systemic diseases and conditions can affect the course of periodontitis or have a negative impact on the periodontal attachment apparatus. Gingival recessions are highly prevalent and often associated with hypersensitivity, the development of caries and non-carious cervical lesions on the exposed root surface and impaired esthetics. Occlusal forces can result in injury of teeth and periodontal attachment apparatus. Several developmental or acquired conditions associated with teeth or prostheses may predispose to diseases of the periodontium. The aim of this working group was to review and update the 1999 classification with regard to these diseases and conditions, and to develop case definitions and diagnostic considerations. METHODS: Discussions were informed by four reviews on 1) periodontal manifestions of systemic diseases and conditions; 2) mucogingival conditions around natural teeth; 3) traumatic occlusal forces and occlusal trauma; and 4) dental prostheses and tooth related factors. This consensus report is based on the results of these reviews and on expert opinion of the participants. RESULTS: Key findings included the following: 1) there are mainly rare systemic conditions (such as Papillon-Lefevre Syndrome, leucocyte adhesion deficiency, and others) with a major effect on the course of periodontitis and more common conditions (such as diabetes mellitus) with variable effects, as well as conditions affecting the periodontal apparatus independently of dental plaque biofilm-induced inflammation (such as neoplastic diseases); 2) diabetes-associated periodontitis should not be regarded as a distinct diagnosis, but diabetes should be recognized as an important modifying factor and included in a clinical diagnosis of periodontitis as a descriptor; 3) likewise, tobacco smoking - now considered a dependence to nicotine and a chronic relapsing medical disorder with major adverse effects on the periodontal supporting tissues - is an important modifier to be included in a clinical diagnosis of periodontitis as a descriptor; 4) the importance of the gingival phenotype, encompassing gingival thickness and width in the context of mucogingival conditions, is recognized and a novel classification for gingival recessions is introduced; 5) there is no evidence that traumatic occlusal forces lead to periodontal attachment loss, non-carious cervical lesions, or gingival recessions; 6) traumatic occlusal forces lead to adaptive mobility in teeth with normal support, whereas they lead to progressive mobility in teeth with reduced support, usually requiring splinting; 7) the term biologic width is replaced by supracrestal tissue attachment consisting of junctional epithelium and supracrestal connective tissue; 8) infringement of restorative margins within the supracrestal connective tissue attachment is associated with inflammation and/or loss of periodontal supporting tissue. However, it is not evident whether the negative effects on the periodontium are caused by dental plaque biofilm, trauma, toxicity of dental materials or a combination of these factors; 9) tooth anatomical factors are related to dental plaque biofilm-induced gingival inflammation and loss of periodontal supporting tissues. CONCLUSION: An updated classification of the periodontal manifestations and conditions affecting the course of periodontitis and the periodontal attachment apparatus, as well as of developmental and acquired conditions, is introduced. Case definitions and diagnostic considerations are also presented.

Increased levels of soluble CD163 in periodontitis patients.

AIM: Soluble CD163 (sCD163) has been implicated as a new biomarker in inflammatory conditions. The aim of this cross-sectional study was to assess CD163 levels systemically and locally in patients with chronic periodontitis. METHODS: sCD163 levels were measured by ELISA in serum samples from 70 periodontitis and 70 periodontally healthy subjects, and in saliva samples in a subset of the population. Two gingival biopsies were harvested per subject from 20 periodontitis patients: one from a periodontally affected site, the other from a healthy site, and the relative expression of CD163 mRNA was assessed by real-time PCR. RESULTS: Serum sCD163 was significantly higher in periodontitis patients compared to periodontally healthy subjects (720.0 ± 330.6 ng/ml versus 510.7 ± 219.6 ng/ml, respectively; p < .001). Similarly, sCD163 levels in saliva were significantly increased in periodontitis compared to healthy subjects (3.01 ± 5.07 ng/ml versus 1.98 ± 4.95 ng/ml, respectively; p = .009). Serum and saliva sCD163 levels showed a positive correlation (Kendall's tau .27, p = .018). Importantly, CD163 gene expression was significantly higher in affected sites compared to unaffected sites in periodontitis patients, with a mean fold upregulation of 9.9 (STD: 15.3, p = .010). CONCLUSION: Our findings suggest that CD163 may be involved in the pathogenesis of periodontitis and its link with systemic conditions.

Six-month outcomes in dental patients identified with hyperglycaemia: a randomized clinical trial.

AIM: To assess an approach to improving behavioural and glycaemic outcomes in dental patients who present with diabetes risk factors and previously unrecognized hyperglycaemia. METHODS: We randomized 101 individuals identified with potential diabetes or pre-diabetes into two interventions. In the basic/control intervention, participants were informed about their diabetes risk factors and blood test result, and advised to see a physician. In the enhanced/test intervention, patients received a detailed explanation of findings and their implications, a written report for the physician, and were contacted at 2 and 4 months to inquire whether medical follow-up had occurred. At a 6-month re-evaluation, outcome measures included visit to physician, positive lifestyle changes and reduction in HbA1c. RESULTS: Seventy-three subjects returned for the 6-month visit. The two intervention groups did not significantly differ in any of the outcome variables. Eighty-four percent of subjects reported having visited a physician post-randomization, and 49% reported at least one positive lifestyle change as a result of our intervention. In subjects identified with potential diabetes (baseline HbA1c ≥ 6.5%), HbA1c was reduced 1.46 ± 0.28% compared to baseline (p < 0.01). CONCLUSION: Diabetes risk assessment and education by dental professionals of affected individuals unaware of their status may contribute to improved patient outcomes.

Periodontal findings in individuals with newly identified pre-diabetes or diabetes mellitus.

AIM: To assess the periodontal status and number of missing teeth in patients with newly identified pre-diabetes or diabetes mellitus. METHODS: A total of 1097 subjects with previously undiagnosed diabetes were available for study, and were categorized into normoglycaemic, potentially pre-diabetes or potentially diabetes groups based on a point-of-care (POC) HbA1c test. RESULTS: In fully adjusted models, significant differences were observed between all groups for the per cent of teeth with at least one site with a probing depth of ≥5 mm. For bleeding on probing, there were significant differences between diabetes and pre-diabetes (p = 0.001), and between diabetes and normoglycaemic groups (p = 0.002). For missing teeth, there were significant differences between the pre-diabetes and normoglycaemic groups (p = 0.034), and the diabetes and normoglycaemic groups (p = 0.004). CONCLUSIONS: Individuals with previously unidentified pre-diabetes demonstrate a level of periodontal destruction between that observed for normoglycaemic individuals and persons with diabetes. These data emphasize the association of oral findings to dysglycaemia, and suggest that periodontal disease and tooth loss can be early complications of diabetes mellitus.

A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes.

AIMS: To review the evidence for the molecular and cellular processes that may potentially link periodontal disease and diabetes. The pathogenic roles of cytokines and metabolic molecules (e.g. glucose, lipids) are explored and the role of periodontal bacteria is also addressed. Paradigms for bidirectional relationships between periodontitis and diabetes are discussed and opportunities for elaborating these models are considered. METHODS: Database searches were performed using MeSH terms, keywords, and title words. Studies were evaluated and summarized in a narrative review. RESULTS: Periodontal microbiota appears unaltered by diabetes and there is little evidence that it may influence glycaemic control. Small-scale clinical studies and experiments in animal models suggest that IL-1ß, TNF-α, IL-6, OPG and RANKL may mediate periodontitis in diabetes. The AGE-RAGE axis is likely an important pathway of tissue destruction and impaired repair in diabetes-associated periodontitis. A role for locally activated pro-inflammatory factors in the periodontium, which subsequently impact on diabetes, remains speculative. CONCLUSION: There is substantial information on potential mechanistic pathways which support a close association between diabetes and periodontitis, but there is a real need for longitudinal clinical studies using larger patient groups, integrated with studies of animal models and cells/tissues in vitro.

Klebsiella pneumoniae induces an inflammatory response in human retinal-pigmented epithelial cells.

PURPOSE: The retinal pigment epithelium (RPE) is a barrier to Klebsiella pneumoniae infection in endogenous endophthalmitis. Nevertheless, the inflammatory response of RPE cells upon interaction with this pathogen has not been studied. Here we tested the hypothesis that K. pneumoniae induces an inflammatory response in human retinal epithelial cells. METHODS: In this study we set out to investigate the effects of whole K. pneumoniae and of its lipopolysaccharide on RPE cells in vitro using bacterial invasion and cytotoxicity assays, fluorescent microscopy and ELISA. For that, we utilized K. pneumoniae strain ATCC 43816 and the continuous human retinal-pigmented epithelial cell line ARPE-19. RESULTS: Stimulation of ARPE-19 with live K. pneumoniae for 24h induced a 31.5-fold (p=0.0132) increase in IL-6 and 6.5-fold (p=0.0004) increase in MCP-1 levels compared to the non-infected control cells. Purified K. pneumoniae LPS (1µgml(-1)) also induced cytokine levels, MCP-1 (1.7-fold upregulation; p=0.0006) and IL-6 (1.3-fold upregulation, p=0.065). The tested K. pneumoniae strain ATCC 43816 did not have a significant effect on the viability of ARPE-19 cells (11% decrease, p=0.096) and showed a low ability to invade the cells. CONCLUSIONS: Both whole live K. pneumoniae and K. pneumoniae LPS exert a strong pro-inflammatory effect on retinal pigmented epithelial cells, consistent with clinical manifestations of disease. Bacterial pro-inflammatory effects are not likely related to host cell invasion. This is the first investigation of the interactions of a major endogenous endophthalmitis pathogen, K. pneumoniae with human retinal pigmented epithelial cells.

Vascular and inflammatory stresses mediate atherosclerosis via RAGE and its ligands in apoE-/- mice.

Endothelial dysfunction is a key triggering event in atherosclerosis. Following the entry of lipoproteins into the vessel wall, their rapid modification results in the generation of advanced glycation endproduct epitopes and subsequent infiltration of inflammatory cells. These inflammatory cells release receptor for advanced glycation endproduct (RAGE) ligands, specifically S100/calgranulins and high-mobility group box 1, which sustain vascular injury. Here, we demonstrate critical roles for RAGE and its ligands in vascular inflammation, endothelial dysfunction, and atherosclerotic plaque development in a mouse model of atherosclerosis, apoE-/- mice. Experiments in primary aortic endothelial cells isolated from mice and in cultured human aortic endothelial cells revealed the central role of JNK signaling in transducing the impact of RAGE ligands on inflammation. These data highlight unifying mechanisms whereby endothelial RAGE and its ligands mediate vascular and inflammatory stresses that culminate in atherosclerosis in the vulnerable vessel wall.

Oral disease experience of older adults seeking oral health services.

OBJECTIVE: The objective of this investigation was to describe the dental disease (dental caries and alveolar bone loss) experience in a sample of community-dwelling older adults who regularly utilize dental services in New York City. BACKGROUND: Public financing for dental care directed at older adults in the United States is minimal. Improved preventive methods, primarily the use of fluorides, have resulted in declines in tooth loss, and concomitant increase in risk for dental diseases among older adults. While the oral disease burden in institutionalized elderly and those unable to access services is well-documented, the dental care needs of older adults who access dental services are not well documented. MATERIALS AND METHODS: Radiographic and record review were used to determine prevalence of dental caries, alveolar bone loss, frequency of service utilization, and medical status in this cross-sectional investigation of a sample of older adults (N = 200) using dental services at Columbia University College of Dental Medicine. RESULTS: Only 9% of the sample was completely edentulous, the mean DMFT was 19.9 and mean alveolar bone loss was 3.6 mm. Missing and Decayed Teeth accounted for 57.8% and 6.5% of the total caries burden respectively. Missing Teeth and alveolar bone loss increased with increasing age, but there was no increase in Decayed Teeth. CONCLUSIONS: While access to and utilization of dental services may result in improved tooth retention, older adults who use dental services continue to have dental care needs, especially periodontal care needs.

Disruption of Monocyte and Macrophage Homeostasis in Periodontitis.

Monocytes and macrophages are major cellular components of the innate immunity that play essential roles in tissue homeostasis. The contribution of different subsets of monocytes/macrophages to periodontal health and disease has not been fully elucidated. Type 2 diabetes mellitus (T2DM) is a risk factor for periodontitis. We hypothesized that the monocyte/macrophage signaling is perturbed in periodontitis-affected sites versus periodontally healthy sites and that this perturbation plays a critical role in the pathogenesis of periodontitis. Pairs of gingival tissue samples (each from a periodontally healthy and a periodontitis-affected site of the same patient) were harvested from 27 periodontitis patients, with and without T2DM. Each sample was processed to form a single-cell suspension, and a flow-cytometry panel was designed and validated to study monocyte and macrophage phenotypes. In separate experiments, the transcriptional changes associated with a pro-inflammatory phenotype were also examined in monocyte/macrophage subsets obtained from peripheral blood of patients with T2DM versus diabetes-free controls. A significantly higher proportion of intermediate (CD14+CD16+) monocytes was observed in periodontitis-affected tissues compared to healthy tissues. These monocytes overexpressed HLA-DR and PDL1 molecules, suggesting their activated inflammatory status. PDL1 increase was specific to intermediate monocytes. The ratio of M1/M2 macrophages was also significantly higher in periodontally affected sites, signifying an imbalance between inflammatory and repair mechanisms. We found a significantly higher expression of PDL1 in overall monocytes and M1 macrophages in periodontitis-affected sites compared to controls. Importantly, we identified a subpopulation of M1 macrophages present in periodontally affected tissues which expressed high levels of CD47, a glycoprotein of the immunoglobulin family that plays a critical role in self-recognition and impairment of phagocytosis. Analysis of the transcriptional landscape of monocytes/macrophages in gingival tissue of T2DM patients with periodontitis revealed a significant disruption in homeostasis toward a proinflammatory phenotype, elevation of pro-inflammatory transcription factors STAT1 and IRF1, and repression of anti-inflammatory JMJD3 in circulating monocytes. Taken together, our results demonstrate disruption of myeloid-derived cell homeostasis in periodontitis, with or without T2DM, and highlight a potentially significant role of these cell types in its pathogenesis. The impact of macrophage and monocyte signaling pathways on the pathobiology of periodontitis should be further evaluated.

Porphyromonas gingivalis infection and prothrombotic effects in human aortic smooth muscle cells.

INTRODUCTION: Accumulating evidence has demonstrated an association between periodontal infectious agents, such as Porphyromonas gingivalis, and vascular disease. Tissue factor (TF) and its specific tissue factor pathway inhibitor (TFPI) are produced by vascular cells and are important regulators of the coagulation cascade. MATERIALS AND METHODS: To assess the role of P. gingivalis in atherothrombosis, we infected primary human aortic smooth muscle cells (HASMC) with either P. gingivalis 381, its non-invasive mutant DPG3, or heat-killed P. gingivalis 381. Levels and activity of TF and TFPI were measured 8 and 24 hours after infection in cell extracts and cell culture supernatants. RESULTS: P. gingivalis 381 did not affect total TF antigen or TF activity in HASMC, but it significantly suppressed TFPI levels and activity compared to uninfected control cells, and those infected with the non-invasive mutant strain or the heat-killed bacteria. Further, P. gingivalis' LPS (up to a concentration of 5 microg/ml) failed to induce prothrombotic effects in HASMC, suggesting a significant role for the ability of whole viable bacteria to invade this cell type. CONCLUSION: These data demonstrate for the first time that infection with a periodontal pathogen induces a prothrombotic response in HASMC.

Heterogeneity of systemic inflammatory responses to periodontal therapy.

AIMS: We investigated the effect of comprehensive periodontal therapy on the levels of multiple systemic inflammatory biomarkers. MATERIAL AND METHODS: Thirty patients with severe periodontitis received comprehensive periodontal therapy within a 6-week period. Blood samples were obtained at: 1-week pre-therapy (T1), therapy initiation (T2), treatment completion (T3), and 4 weeks thereafter (T4). We assessed the plasma concentrations of 19 biomarkers using multiplex assays, and serum IgG antibodies to periodontal bacteria using checkerboard immunoblotting. At T2 and T4, dental plaque samples were analysed using checkerboard hybridizations. RESULTS: At T3, PAI-1, sE-selectin, sVCAM-1, MMP-9, myeloperoxidase, and a composite summary inflammatory score (SIS) were significantly reduced. However, only sE-selectin, sICAM, and serum amyloid P sustained a reduction at T4. Responses were highly variable: analyses of SIS slopes between baseline and T4 showed that approximately 1/3 and 1/4 of the patients experienced a marked reduction and a pronounced increase in systemic inflammation, respectively, while the remainder were seemingly unchanged. Changes in inflammatory markers correlated poorly with clinical, microbiological and serological markers of periodontitis. CONCLUSIONS: Periodontal therapy resulted in an overall reduction of systemic inflammation, but the responses were inconsistent across subjects and largely not sustainable. The determinants of this substantial heterogeneity need to be explored further.

Impact of connective tissue graft thickness on surgical outcomes: A pilot randomized clinical trial.

BACKGROUND: The aim of this study was to compare thick versus thin connective tissue grafts (CTG) for the treatment of gingival recession, over a 3-month period. METHODS: Forty-two CTG procedures were performed on single tooth Miller Class I or II recession defects at either premolar or anterior sites in 30 individuals. Procedures were randomized (1:1 ratio) to CTG thickness of 1 or 2 mm (parallel group design). Primary outcomes were the change in the width of the zone of keratinized tissue and the amount of root coverage achieved 3 months postoperatively at the recipient site. Secondary outcomes included change in the thickness of keratinized tissue at 3 months and patient-reported outcomes, such as pain, bleeding, and swelling at both the recipient and donor sites at 1 week, 2 weeks, 1 month, and 3 months. RESULTS: No significant differences were found between the two groups for any of the primary or secondary outcomes. Mean root coverage achieved was 2.1 ± 0.2 mm in the 1-mm thick group and 2.5 ± 0.2 mm in the 2-mm thick group (P = 0.33). Keratinized tissue width was increased by 2.2 ± 0.2 mm in the 1-mm thick group and by 2.7 ± 0.3 mm in the 2-mm thick group (P = 0.18). Keratinized tissue thickness was increased by 1.0 ± 0.1 mm and by 1.2 ± 0.1 mm in the 1- and 2-mm thick groups, respectively (P = 0.09). CONCLUSION: Within the current study limitations, our results suggest that similar root coverage and increase in the width and thickness of keratinized tissue can be achieved at 3 months whether a 1- or 2-mm thick CTG is used.

Soluble Forms of the Receptor for Advanced Glycation Endproducts (RAGE) in Periodontitis.

The receptor for advanced glycation endproducts (RAGE) is critically involved in the pathobiology of chronic inflammatory diseases. Soluble forms of RAGE have been proposed as biomarkers of severity in inflammatory and metabolic conditions, and in monitoring therapeutic responses. The aim of the present study was to determine circulating levels of the soluble forms of RAGE in periodontitis and to evaluate the expression of cell-bound, full-length RAGE and its antagonist AGER1 locally, in gingival tissues. Periodontitis patients and periodontally healthy, sex- and age-matched controls (50 per group) were included. Serum levels of total soluble RAGE and cleaved RAGE (cRAGE) were significantly lower in periodontitis patients. Levels of the endogenous secretory esRAGE were similar in the two groups. cRAGE remained significantly lower in the periodontitis group following multiple adjustments, and had a statistically significant inverse correlation with body mass index and all periodontal parameters. In periodontitis patients, gene expression of full-length RAGE and of AGER1 were significantly higher in periodontitis-affected gingival tissues compared to healthy gingiva. Soluble forms of RAGE, particularly cRAGE, may serve as biomarkers for the presence and severity/extent of periodontitis, and may be implicated in its pathogenesis and its role as a systemic inflammatory stressor.

Oral disease burden in northern Manhattan patients with diabetes mellitus.

OBJECTIVES: We explored the association between diabetes mellitus and oral disease in a low-socioeconomic-status urban population. METHODS: Dental records of 150 adults with diabetes and 150 nondiabetic controls from the dental clinic at Columbia University in Northern Manhattan matched by age and gender were studied. RESULTS: There was a 50% increase in alveolar bone loss in diabetic patients compared with nondiabetic controls. Diabetes, increasing age, male gender, and use of tobacco products had a statistically significant effect on bone loss. CONCLUSIONS: Our findings provide evidence that diabetes is an added risk for oral disease in this low-income, underserved population of Northern Manhattan. Oral disease prevention and treatment programs may need to be part of the standards of continuing care for patients with diabetes.

Management of patients with diabetes by general dentists in New Zealand.

BACKGROUND: The prevalence of diabetes in New Zealand is reaching epidemic proportions, with serious implications for oral health. We investigated the attitudes, beliefs, and practices of New Zealand (NZ) general dental practitioners (GDPs) with respect to the management of patients with diabetes and contrasted the NZ findings with those from a similar survey of GDPs in the Northeast United States (NE US) conducted in 2002. METHODS: A nationwide postal survey was conducted of NZ dentists. A random sample was selected from the 2005 New Zealand Dental Register. Responses were received from 437 dentists (response rate: 64.5%). RESULTS: The sample was representative. Most GDPs participated in the assessment and discussion phases of managing patients with diabetes, but the prevalence of more hands-on activities (such as testing) was considerably lower. Three-quarters of dentists asked new patients about their type of diabetes. Just over two in five respondents believed that their evaluation and/or management of the patient with diabetes were hindered by the lack of continuing education opportunities. Almost one-third of dentists were unwilling to screen for diabetes using a finger-stick test, and only 2.6% overall had ever done so. There were only minor differences between NZ and NE US dentists. CONCLUSION: Given the increasing numbers of patients with diabetes (known and unknown), there is a need for NZ and US dentists to be more involved in their active management.