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Objective. To investigate the knowledge and practice of tobacco cessation and counseling (TCC) among dental practitioners and their attitude and perceived barriers. Methods. A cross-sectional study targeted licensed dental practitioners in Jeddah, Saudi Arabia. Participants answered a pretested and validated self-administered questionnaire consisted of demographic data; smoking status; knowledge of tobacco hazards, attitude, and practice; and perceived barriers of tobacco cessation counseling. Result. Among the total sample of 529, response rate was 72.2% (mean age ( 34.20 ± 9.38 years ), males (42.4%), and current smokers (23.8%)). Only 13.2% received formal training on TCC. Around (57.1%) reported smoking of dental team as an obstacle for TCC. Half of the participants (49.9%) reported patient’s resistance as barrier to TCC. Others (45%–48%) reported insufficient time, knowledge, or training for TCC. Professional responsibility and willingness to provide cessation services constituted the highest median. Conclusion. The majority showed willingness to participate in TCC. Lack of training, smoking status of providers, females, inadequate materials, and patients’ resistance were the most common barriers. Education and training on TCC are recommended and should be allowed as a routine practice in dentistry.

Purpose The study aimed to determine the types of periodontal services rendered by general dental practitioners (GDPs) in Saudi Arabia. Subjects and methods A cross-sectional survey was performed on a convenience sample of 340 licensed GDPs practicing within Saudi Arabia. GDPs were asked several questions regarding the types of periodontal services offered, the level of training and education received in periodontics and the periodontal referral processes. Results Two hundred and ninety GDPs responded to the survey. The most commonly rendered periodontal services by the GDPs were oral hygiene instructions (84.1%; 244/290), mouthwash prescribing (82.7%; 240/290) and scaling and root planing (72.4%; 210/290). Only 21% (59/282) of the GDPs surveyed reported providing periodontal surgical services. The most frequently rendered surgical procedures included gingivectomy, functional crown lengthening and single posterior implant. Also, 76% (220/290) of the GDPs had no continuing education (CE) credit relating to periodontics. The level of training received in the dental school seemed to be an important factor that influenced a GDP's decision to provide periodontal services. Also, 64% (184/286) of the GDPs were not routinely performing periodontal screening exams. The most common reason for not referring patients to a periodontist was practice setting's policy. Conclusion Periodontal services commonly rendered by the GDPs of this survey were mostly nonsurgical in nature. The results indicate a need for formal advanced training in periodontics. GDPs should be encouraged to take periodontic CE courses.

The aim of this study was to investigate the effect of using subantimicrobial dose doxycycline as an adjunct in periodontitis stage 2, grade B in subjects with type 2 diabetes mellitus. A total of thirty patients were divided into the following two groups with reference to periodontitis, type 2 diabetes mellitus, and administration of the doxycycline drug: Group I: patients with periodontitis stage 2, grade B and type 2 diabetes mellitus who received SRP only. Group II: patients with periodontitis stage 2, grade B and type 2 diabetes mellitus who received SRP and doxycycline 20 mg. The following clinical measurements were recorded at baseline (prior to scaling and root planning) and after one and three months postoperatively: GI, PI, and PD with a periodontal calibrated probe. The levels of both MMP-9 and MMP-13, from 60 GCF samples, were analyzed by ELISA. Patients treated with SRP and doxycycline 20 mg showed a significant reduction of PD, PI, GI, MMP-9, and MMP-13 than patients who received SRP only. Improvements in parameters clinically and biochemically were observed following the adjunctive use of doxycycline subantimicrobial dose therapy for the management of stage 2, grade B periodontitis patients with type 2 diabetes mellitus.

Background Occupational violence is considered unlawful in professional environments worldwide. In the healthcare industry, including dentistry, the safety of workers is essential, and it is of the utmost importance to ensure patient and employee safety and provide quality care. This study aimed to evaluate the prevalence of violence and associated workplace policies among oral healthcare professionals. Additionally, it aimed to identify the factors associated with violence and their impact on oral healthcare workers. Methods A systematic review and analysis of the literature was conducted using PubMed, ScienceDirect, Scopus, Web of Science, Cochrane Library and ProQuest. Original articles written in English and published between January 1992 and August 2019 were included in the analysis. Results A total of 980 articles were found, and eight were selected for analysis. The violence experienced by healthcare workers included both physical and non-physical forms, such as shouting, bullying, and threatening; it also included sexual harassment. The impact of violence on workers manifested as impaired quality of work, psychological problems, and, although rare, quitting the job. With regard to dental healthcare, awareness of occupational violence policies among dental professionals has not been previously reported in the literature. Conclusions The increasing incidence of occupational violence against oral healthcare workers indicates the need for the implementation of better protective measures to create a safe working environment for dental professionals. There is a current need for increasing awareness of workplace violence policies and for the detection and reporting of aggression and violence at dental facilities.

Diabetes increases the likelihood of fracture, interferes with fracture healing and impairs angiogenesis. The latter may be significant due to the critical nature of angiogenesis in fracture healing. Although it is known that diabetes interferes with angiogenesis the mechanisms remain poorly defined. We examined fracture healing in normoglycemic and streptozotocin-induced diabetic mice and quantified the degree of angiogenesis with antibodies to three different vascular markers, CD34, CD31 and Factor VIII. The role of diabetes-enhanced inflammation was investigated by treatment of the TNFα-specific inhibitor, pegsunercept starting 10days after induction of fractures. Diabetes decreased both angiogenesis and VEGFA expression by chondrocytes. The reduced angiogenesis and VEGFA expression in diabetic fractures was rescued by specific inhibition of TNF in vivo. In addition, the TNF inhibitor rescued the negative effect of diabetes on endothelial cell proliferation and endothelial cell apoptosis. The effect of TNFα in vitro was enhanced by high glucose and an advanced glycation endproduct to impair microvascular endothelial cell proliferation and tube formation and to stimulate apoptosis. The effect of TNF, high glucose and an AGE was mediated by the transcription factor FOXO1, which increased expression of p21 and caspase-3. These studies indicate that inflammation plays a major role in diabetes-impaired angiogenesis in endochondral bone formation through its effect on microvascular endothelial cells and FOXO1.

Additional file 1. Quality Assessment Scale for cohort studies adapted from the Newcastle-Ottawa scale.

Background The gingiva is part of the periodontium supporting structures surrounding the teeth and commonly involved in gingival and periodontal conditions. Assessing the distribution of gingival lesions is important for evaluating the prevalence of periodontal disease in the population to optimize the oral health care services. The purpose of this study is to report the frequency and distribution of gingival lesions biopsied from 1996-2016. Material and methods This cross-sectional retrospective study retrieved data from all gingival lesions biopsied from 1996-2016 and sent to the King Abdulaziz University Dental Hospital oral pathology laboratory. Histologic sections were reviewed in a blinded manner by a certified oral pathologist to confirm the initial histologic diagnosis. Results Of the 1,248 oral-maxillofacial lesions, 119 (9.5%) gingival lesions were diagnosed. The mean age was 41.58 years. Gingival lesions were more prevalent in female patients than male patients (53.8%). The most common diagnoses were reactive lesions (41.2%). Pyogenic granuloma was the predominant lesion in the category (n=26, 21.8%), and followed by inflammatory conditions (24.4%), benign neoplasm (9.2%), malignant neoplasm (7.6%), epithelial lesions (7.6%), miscellaneous (5%), and immune-mediated diseases (5%). Squamous cell carcinoma was the only malignant neoplasm reported (7.6%; mean age, 57.44 years) and more common in male than female patients (2:1). Most biopsies were sent from oral and maxillofacial surgeons (55.6%) followed by general dentists (22.2%) and periodontists (12.8%). Conclusions Pyogenic granuloma was the most common gingival lesion. Squamous cell carcinoma was the only malignant lesion in which histologic examination was the definitive diagnostic measure. This study provides information about the frequencies and distributions of gingival lesions over 20 years. Key words:Gingival biopsies, retrospective, reactive lesions, oral pathology.

Diabetes mellitus is a metabolic disorder associated with several complications, including impaired healing. Bone, as important skeletal structure in the body, is affected by the diabetic condition, particularly during fracture healing processes. In this review, we discuss the normal fracture process, as well as mechanical, histological, and molecular negative changes that take place during diabetic fracture repair. Although diabetes affects cartilages and bones from anabolic aspects, our studies have shed light on the impact of diabetes on the catabolic aspect as well. Several underlying proposed mechanisms involved in impaired diabetic fracture healing were also reviewed. Current potential therapeutic agents, which may improve the healing process, were reviewed based on the current understanding of diabetes’ impact on the various stages of fracture healing.

To gain insight into the effect of diabetes on fracture healing, experiments were carried out focusing on chondrocyte apoptosis during the transition from cartilage to bone. Type 1 diabetes was induced in mice by multiple low-dose streptozotocin injections, and simple transverse fractures of the tibia or femur was carried out. Large-scale transcriptional profiling and gene set enrichment analysis were performed to examine apoptotic pathways on total RNA isolated from fracture calluses on days 12, 16, and 22, a period of endochondral bone formation when cartilage is resorbed and chondrocyte numbers decrease. Tumor necrosis factor α (TNF-α) protein levels were assessed by ELISA and caspase-3 by bioactivity assay. The role of TNF was examined by treating mice with the TNF-specific inhibitor pegsunercept. In vitro studies investigated the proapoptotic transcription factor FOXO1 in regulating TNF-induced apoptosis of chondrogenic ATDC5 and C3H10T1/2 cells as representative of differentiated chondrocytes, which are important during endochondral ossification. mRNA profiling revealed an upregulation of gene sets related to apoptosis in the diabetic group on day 16 when cartilage resorption is active but not day 12 or day 22. This coincided with elevated TNF-α protein levels, chondrocyte apoptosis, enhanced caspase-3 activity, and increased FOXO1 nuclear translocation (p < .05). Inhibition of TNF significantly reduced these parameters in the diabetic mice but not in normoglycemic control mice (p < .05). Silencing FOXO1 using siRNA in vitro significantly reduced TNF-induced apoptosis and caspase activity in differentiated chondrocytes. The mRNA levels of the proapoptotic genes caspase-3, caspase-8, caspase-9, and TRAIL were significantly reduced with silencing of FOXO1 in chondrocytic cells. Inhibiting caspase-8 and caspase-9 significantly reduced TNF-induced apoptosis in chondrogenic cells. These results suggest that diabetes causes an upregulation of proapoptotic genes during the transition from cartilage to bone in fracture healing. Diabetes increased chondrocyte apoptosis through a mechanism that involved enhanced production of TNF-α, which stimulates chondrocyte apoptosis and upregulates mRNA levels of apoptotic genes through FOXO1 activation. © 2010 American Society for Bone and Mineral Research.

Diabetes interferes with fracture repair; therefore, we investigated mechanisms of impaired fracture healing in a model of multiple low-dose streptozotocin-induced diabetes. Microarray and gene set enrichment analysis revealed an up-regulation of gene sets related to inflammation, including tumor necrosis factor (TNF) signaling in the diabetic group, when cartilage is being replaced by bone on day 16, but not on days 12 or 22. This change coincided with elevated osteoclast numbers and accelerated removal of cartilage in the diabetic group (P < 0.05), which was reflected by smaller callus size. When diabetic mice were treated with the TNF-specific inhibitor, pegsunercept, the number of osteoclasts, cartilage loss, and number of TNF-alpha and receptor activator for nuclear factor kB ligand positive chondrocytes were significantly reduced (P < 0.05). The transcription factor forkhead box 01 (FOXO1) was tested for mediating TNF stimulation of osteoclastogenic and inflammatory factors in bone morphogenetic protein 2 pretreated ATDC5 and C3H10T1/2 chondrogenic cells. FOXO1 knockdown by small-interfering RNA significantly reduced TNF-alpha, receptor activator for nuclear factor kB ligand, macrophage colony-stimulating factor, interleukin-1alpha, and interleukin-6 mRNA compared with scrambled small-interfering RNA. An association between FOXO1 and the TNF-alpha promoter was demonstrated by chromatin immunoprecipitation assay. Moreover, diabetes increased FOXO1 nuclear translocation in chondrocytes in vivo and increased FOXO1 DNA binding activity in diabetic fracture calluses (P < 0.05). These results suggest that diabetes-enhanced TNF-alpha increases the expression of resorptive factors in chondrocytes through a process that involves activation of FOXO1 and that TNF-alpha dysregulation leads to enhanced osteoclast formation and accelerated loss of cartilage.

Diabetes interferes with bone formation and impairs fracture healing, an important complication in humans and animal models. The aim of this study was to examine the impact of diabetes on mesenchymal stem cells (MSCs) during fracture repair.Fracture of the long bones was induced in a streptozotocin-induced type 1 diabetic mouse model with or without insulin or a specific TNFα inhibitor, pegsunercept. MSCs were detected with cluster designation-271 (also known as p75 neurotrophin receptor) or stem cell antigen-1 (Sca-1) antibodies in areas of new endochondral bone formation in the calluses. MSC apoptosis was measured by TUNEL assay and proliferation was measured by Ki67 antibody. In vitro apoptosis and proliferation were examined in C3H10T1/2 and human-bone-marrow-derived MSCs following transfection with FOXO1 small interfering (si)RNA.Diabetes significantly increased TNFα levels and reduced MSC numbers in new bone area. MSC numbers were restored to normal levels with insulin or pegsunercept treatment. Inhibition of TNFα significantly reduced MSC loss by increasing MSC proliferation and decreasing MSC apoptosis in diabetic animals, but had no effect on MSCs in normoglycaemic animals. In vitro experiments established that TNFα alone was sufficient to induce apoptosis and inhibit proliferation of MSCs. Furthermore, silencing forkhead box protein O1 (FOXO1) prevented TNFα-induced MSC apoptosis and reduced proliferation by regulating apoptotic and cell cycle genes.Diabetes-enhanced TNFα significantly reduced MSC numbers in new bone areas during fracture healing. Mechanistically, diabetes-enhanced TNFα reduced MSC proliferation and increased MSC apoptosis. Reducing the activity of TNFα in vivo may help to preserve endogenous MSCs and maximise regenerative potential in diabetic patients.

Chemokines are thought to play an important role in several aspects of bone metabolism including the recruitment of leukocytes and the formation of osteoclasts. We investigated the impact of diabetes on chemokine expression in normal and diabetic fracture healing. Fracture of the femur was performed in streptozotocin-induced diabetic and matched normoglycemic control mice. Microarray analysis was carried out and chemokine mRNA levels in vivo were assessed. CCL4 were examined in fracture calluses by immunohistochemistry and the role of TNF in diabetes-enhanced expression was investigated by treatment of animals with the TNF-specific inhibitor, pegsunercept. In vitro studies were conducted with ATDC5 chondrocytes. Diabetes significantly upregulated mRNA levels of several chemokines in vivo including CCL4, CCL8, CCL6, CCL11, CCL20, CCL24, CXCL2, CXCL5 and chemokine receptors CCR5 and CXCR4. Chondrocytes were identified as a significant source of CCL4 and its expression in diabetic fractures was dependent on TNF in diabetic fractures (P

Fracture healing in diabetic individuals and in animal models of diabetes is impaired. To investigate mechanisms by which diabetes may affect fracture healing we focused on the transition from cartilage to bone, a midpoint in the fracture healing process. Femoral fractures were induced in mice rendered diabetic by multiple low dose streptozotocin treatment and compared to matching normoglycemic mice. One group of diabetic animals was treated with slow release insulin to maintain normal serum glucose levels. The results indicate that there was relatively little difference in the initial formation of the fracture callus on day 10. However, on day 16 the diabetic group had significantly smaller callus, greater loss of cartilage and enhanced osteoclastogenesis that was normalized by treatment with insulin when assessed by histomorphometric analysis. Chondrocyte apoptosis was significantly higher in diabetic mice and this increase was blocked by insulin. These changes were accompanied by diabetes-increased mRNA levels of RANKL, TNF-alpha, and ADAMTS-4 and -5 measured by real-time PCR, which was reversed by insulin treatment. On days 16 and 22 bone formation within the callus of diabetic mice was significantly less than the normoglycemic and brought to normal levels by insulin treatment. These results suggest that a significant effect of diabetes on fracture healing is increased chondrocyte apoptosis and osteoclastogenesis that accelerates the loss of cartilage and reduces the anlage for endochondral bone formation during fracture repair. That insulin reverses these effects demonstrates that they are directly related to the diabetic condition.