The balance between bone resorption and bone formation is vital for maintenance and regeneration of alveolar bone and supporting structures around teeth and dental implants. Tissue regeneration in ...the oral cavity is regulated by multiple cell types, signaling mechanisms, and matrix interactions. A goal for periodontal tissue engineering/regenerative medicine is to restore oral soft and hard tissues through cell, scaffold, and/or signaling approaches to functional and aesthetic oral tissues. Bony defects in the oral cavity can vary significantly, ranging from smaller intrabony lesions resulting from periodontal or peri-implant diseases to large osseous defects that extend through the jaws as a result of trauma, tumor resection, or congenital defects. The disparity in size and location of these alveolar defects is compounded further by patient-specific and environmental factors that contribute to the challenges in periodontal regeneration, peri-implant tissue regeneration, and alveolar ridge reconstruction. Efforts have been made over the last few decades to produce reliable and predictable methods to stimulate bone regeneration in alveolar bone defects. Tissue engineering/regenerative medicine provide new avenues to enhance tissue regeneration by introducing bioactive models or constructing patient-specific substitutes. This review presents an overview of therapies (e.g., protein, gene, and cell based) and biomaterials (e.g., resorbable, nonresorbable, and 3-dimensionally printed) used for alveolar bone engineering around teeth and implants and for implant site development, with emphasis on most recent findings and future directions.
Periodontal infections have been associated with a state of chronic inflammation. To ascertain whether severe periodontitis and its treatment are associated with oxidative stress, we recruited 145 ...cases (periodontitis) and 56 controls in a case-control study. A further pilot intervention study of 14 cases (periodontal therapy) was performed. Blood samples were taken at baseline (case-control) and 1, 3, 5, 7, and 30 days after treatment (intervention). Diacron-reactive oxygen metabolites (D-ROM), anti-oxidant potential, C-reactive protein (CRP), interleukin-6, and lipid profiles were determined with high-sensitivity assays in serum. Patients with severe periodontitis exhibited higher D-ROM levels (P < 0.001) and lower total anti-oxidant capacity (P < 0.001) compared with healthy control individuals. These findings were independent of age, gender, smoking habits, ethnicity, and standard lipids differences. D-ROM levels were positively correlated with CRP (R = 0.4, P < 0.001) and clinical periodontal parameters (R = 0.20, P < 0.05). Acute increases of D-ROM (P < 0.01) were observed following periodontal therapy. Analysis of these data suggests a positive association between severe periodontitis and oxidative stress.
The aim of this study was to systematically appraise the existing literature on the yet-unclear heritability of gingivitis and periodontitis. This review was conducted following the PRISMA ...guidelines. A search was conducted through the electronic databases Medline, Embase, LILACS, Cochrane Library, Open Grey, Google Scholar, and Research Gate, as complemented by a hand search, for human studies reporting measures of heritability of gingivitis and periodontitis. A total of 9,037 papers were initially identified from combined databases and 10,810 on Google Scholar. After full-text reading, 28 articles met the inclusion criteria and were carried forward to data abstraction. The reviewed data included information from >50,000 human subjects. Meta-analyses were performed by grouping studies based on design and outcome. Heritability (H2) of periodontitis was estimated at 0.38 (95% CI, 0.34 to 0.43; I2 = 12.9%) in twin studies, 0.15 (95% CI, 0.06 to 0.24; I2 = 0%) in other family studies, and 0.29 (95% CI, 0.21 to 0.38; I2 = 61.2%) when twin and other family studies were combined. Genome-wide association studies detected a lower heritability estimate of 0.07 (95% CI, −0.02 to 0.15) for combined definitions of periodontitis, increasing with disease severity and when the interaction with smoking was included. Furthermore, heritability tended to be lower among older age groups. Heritability for the self-reported gingivitis trait was estimated at 0.29 (95% CI, 0.22 to 0.36; I2 = 37.6%), while it was not statistically significant for clinically measured gingivitis. This systematic review brings forward summary evidence to confirm that up to a third of the periodontitis variance in the population is due to genetic factors. This seems consistent across the different studied populations and increases with disease severity. In summary, up to a third of the variance of periodontitis in the population is due to genetic factors, with higher heritability for more severe disease.
Oral Diseases (2012) 18, 236–243
Interleukin‐6 (IL‐6) is a pleomorphic cytokine involved in a number of physiologic and pathologic processes including response to trauma and infection and development ...and progression of inflammation and malignancy. IL‐6 is emerging as an important mediator and novel therapeutic target for chronic inflammatory diseases and cancer. The present study reviews the available evidence regarding the association between IL‐6 and a range of oral diseases including infections (periodontal disease and endodontic infections), immunologically mediated disorders (oral lichen planus and Sjögren’s syndrome) and malignancy (oral cancer and precancer). The role of common genetic variants of IL‐6 in determining individual susceptibility to certain oral diseases, as well as novel therapeutic strategies based on IL‐6 inhibition are also discussed.
Severe periodontitis has been associated with increased systemic inflammation. In a three-arm preliminary randomized trial, we investigated the impact of standard (SPT) and intensive periodontal ...therapy (IPT) on serum inflammatory markers and cholesterol levels. Medical and periodontal parameters, C-reactive protein (CRP), interleukin-6 (IL-6), total cholesterol, and LDL cholesterol were evaluated in 65 systemically healthy subjects suffering from severe generalized periodontitis. Two months after treatment, both SPT and IPT resulted in significant reductions in serum CRP compared with the untreated control (0.5 ± 0.2 mg/L for SPT, P = 0.030 and 0.8 ± 0.2 mg/L for IPT, P = 0.001). Similar results were observed for IL-6. Changes in inflammation were independent of age, gender, body mass index, and ethnicity, but a significant interaction between cigarette smoking and treatment regimen was found. The IPT group also showed a decrease in total and LDL cholesterol after 2 months. Analysis of these data indicates that periodontitis causes moderate systemic inflammation in systemically healthy subjects.
To identify (i) the prevalence of meeting the endpoints of 'stable periodontitis' (probing pocket depth PPD ≤ 4 mm, bleeding on probing BoP < 10%, no BoP at 4 mm sites), 'endpoints of therapy' (no ...PPD > 4 mm with BoP, no PPD ≥ 6 mm), 'controlled periodontitis' (≤4 sites with PPD ≥ 5 mm), 'PPD < 5 mm' and 'PPD < 6 mm' at the start of supportive periodontal care SPC) and (ii) the incidence of tooth loss in relation to not meeting these endpoints within a minimum of 5 years of SPC.
Systematic electronic and manual searches were conducted to identify studies where subjects, upon completion of active periodontal therapy, entered into SPC. Duplicate screening was performed to find relevant articles. Corresponding authors were contacted to confirm inclusion and retrieve required clinical data for further analyses to assess the prevalence of reaching endpoints and incidence of subsequent tooth loss, if available, within at least 5 years of SPC. Meta-analyses were carried out to evaluate risk ratios for tooth loss in relation to not reaching the various endpoints.
Fifteen studies including 12,884 patients and 323,111 teeth were retrieved. Achievement of endpoints at baseline SPC was rare (1.35%, 11.00% and 34.62%, respectively, for 'stable periodontitis', 'endpoints of therapy' and 'controlled periodontitis'). Less than a third of the 1190 subjects with 5 years of SPC data lost teeth-a total of 3.14% of all teeth were lost. Statistically significant associations with tooth loss, at the subject-level, were found for not achieving 'controlled periodontitis' (relative risk RR = 2.57), PPD < 5 mm (RR = 1.59) and PPD < 6 mm (RR = 1.98).
An overwhelming majority of subjects and teeth do not achieve the proposed endpoints for periodontal stability, yet most periodontal patients preserve most of their teeth during an average of 10-13 years in SPC.
COVID-19 has impacted dentistry in unprecedented ways.
The following research aimed to investigate the impact of the COVID-19 pandemic on periodontal practice in the United Kingdom using the COM-B ...(Capability Opportunity Motivation-Behaviour) model as the basis for a questionnaire.
An online survey link was sent to all members of the British Society of Periodontology and Implant Dentistry. A total of 358 responses were received and analysed.
The great majority of participants thought that the pandemic had an impact on their profession, while only 4.7 % had no concerns. The main worries related to financial concerns and ability to provide appropriate levels of care. More than 80 % of respondents agreed that their establishment was compliant with infection control procedures. Some participants felt benefits mainly in terms of more time for CPD activities. It was felt that some of the changes needed will need to be sustained long-term.
Respondents were generally worried. However, they perceived they had the physical and psychological ability to effect changes to their practice, higher than the physical and social opportunities that they were afforded. Although the COVID-19 pandemic is causing profound changes and worries for the profession of Periodontology, clinicians are clear about their capability to control the situation and feel they have the motivation to make the required changes.
COVID-19 has presented clinicians with novel challenges. Investigating the professional response to change and expected impact is of interest in the current climate as we navigate the ‘new normal’. Assessing the results could be useful in informing support strategies moving forward.
Body mass index (BMI) and obesity are associated with the prevalence, extent, and severity of periodontitis. This study investigated the predictive role of overweight/obesity on clinical response ...following non-surgical periodontal therapy in patients with severe periodontitis. Two hundred sixty adults received an intensive course of non-surgical periodontal therapy. Periodontal status at baseline and 2 months was based upon probing pocket depths (PPD), clinical attachment levels (CAL), and whole-mouth gingival bleeding (FMBS) as assessed by two calibrated examiners. Generalized estimating equations (GEE) were used to estimate the impact of BMI and overweight/obesity on periodontal treatment response while controlling for baseline status, age, smoking status (smoker or non-smoker), and full-mouth dental plaque score. BMI (continuous variable) and obesity (vs. normal weight) were associated with worse mean PPD (p < .005), percentage of PPD > 4 mm (p = .01), but not with FMBS (p > .05) or CAL (p > .05) at 2 months, independent of age, smoking status, or dental plaque levels. The magnitude of this association was similar to that of smoking, which was also linked to a worse clinical periodontal outcome (p < .01). BMI and obesity appear to be independent predictors of poor response following non-surgical periodontal therapy.
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