Periodontal Disease Treatment After Stroke or Transient Ischemic Attack: The PREMIERS Study, a Randomized Clinical Trial.

BACKGROUND: Patients with stroke/transient ischemic attack and periodontal disease (PD) are at increased risk for cardiovascular events. PD treatments that can improve stroke risk factors were tested if they might assist patients with cerebrovascular disease. METHODS: In this multicenter phase II trial, patients with stroke/transient ischemic attack and moderately severe PD were randomly assigned to intensive or standard PD treatment arms. The primary outcome measure was a composite of death, myocardial infarction, and recurrent stroke, as well as adverse events. Secondary outcome included changes in stroke risk factors. RESULTS: A total of 1209 patients with stroke/transient ischemic attack were screened, of whom 481 met the PD eligibility criteria; 280 patients were randomized to intensive arm (n=140) and standard arm (n=140). In 12-month period, primary outcome occurred in 11 (8%) in the intensive arm and 17 (12%) in the standard arm. The intensive arm was nonsuperior to the standard arm (hazard ratio, 0.65 [95% CI, 0.30-1.38]) with similar rates of adverse events (sepsis 2.1% versus 0.7%; dental bleeding 1.4% versus 0%; and infective endocarditis 0.7% versus 0%). Secondary-outcome improvements were noted in both arms with diastolic blood pressure and high-density lipoprotein cholesterol (P<0.05). CONCLUSIONS: In patients with recent stroke/transient ischemic attack and PD, intensive PD treatment was not superior to standard PD treatment in prevention of stroke/myocardial infarction/death. Fewer events were noted in the intensive arm and the 2 arms were comparable in the safety outcomes. Secondary-outcome measures showed a trend toward improvement, with significant changes noted in diastolic blood pressure and high-density lipoprotein in both the treatment arms.

Screening of Hydroxyapatite Biomaterials for Alveolar Augmentation Using a Rat Calvaria Critical-Size Defect Model: Bone Formation/Maturation and Biomaterials Resolution.

BACKGROUND: Natural (bovine-/equine-/porcine-derived) or synthetic hydroxyapatite (HA) biomaterials appear to be the preferred technologies among clinicians for bone augmentation procedures in preparation for implant dentistry. The aim of this study was to screen candidate HA biomaterials intended for alveolar ridge augmentation relative to their potential to support local bone formation/maturation and to assess biomaterial resorption using a routine critical-size rat calvaria defect model. METHODS: Eighty adult male Sprague Dawley outbred rats obtained from a approved-breeder, randomized into groups of ten, were used. The calvaria defects (ø8 mm) either received sham surgery (empty control), Bio-Oss (bovine HA/reference control), or candidate biomaterials including bovine HA (Cerabone, DirectOss, 403Z013), and bovine (403Z014) or synthetic HA/ß-TCP (Reprobone, Ceraball) constructs. An 8 wk healing interval was used to capture the biomaterials' resolution. RESULTS: All biomaterials displayed biocompatibility. Strict HA biomaterials showed limited, if any, signs of biodegradation/resorption, with the biomaterial area fraction ranging from 22% to 42%. Synthetic HA/ß-TCP constructs showed limited evidence of biodegradation/erosion (biomaterial area fraction ≈30%). Mean linear defect closure in the sham-surgery control approximated 40%. Mean linear defect closure for the Bio-Oss reference control approximated 18% compared with 15-35% for the candidate biomaterials without significant differences between the controls and candidate biomaterials. CONCLUSIONS: None of the candidate HA biomaterials supported local bone formation/maturation beyond the native regenerative potential of this rodent model, pointing to their limitations for regenerative procedures. Biocompatibility and biomaterial dimensional stability could suggest their potential utility as long-term defect fillers.

Systemic Dietary Hesperidin Modulation of Osteoclastogenesis, Bone Homeostasis and Periodontal Disease in Mice.

This study aimed to evaluate the effects of hesperidin (HE) on in vitro osteoclastogenesis and dietary supplementation on mouse periodontal disease and femoral bone phenotype. RAW 264.7 cells were stimulated with RANKL in the presence or absence of HE (1, 100 or 500 µM) for 5 days, and evaluated by TRAP, TUNEL and Western Blot (WB) analyses. In vivo, C57BL/6 mice were given HE via oral gavage (125, 250 and 500 mg/kg) for 4 weeks. A sterile silk ligature was placed between the first and second right maxillary molars for 10 days and microcomputed tomography (µCT), histopathological and immunohistochemical evaluation were performed. Femoral bones subjected or not to dietary HE (500 mg/kg) for 6 and 12 weeks were evaluated using µCT. In vitro, HE 500 µM reduced formation of RANKL-stimulated TRAP-positive(+) multinucleated cells (500 µM) as well as c-Fos and NFATc1 protein expression (p < 0.05), markers of osteoclasts. In vivo, dietary HE 500 mg/kg increased the alveolar bone resorption in ligated teeth (p < 0.05) and resulted in a significant increase in TRAP+ cells (p < 0.05). Gingival inflammatory infiltrate was greater in the HE 500 mg/kg group even in the absence of ligature. In femurs, HE 500 mg/kg protected trabecular and cortical bone mass at 6 weeks of treatment. In conclusion, HE impaired in vitro osteoclastogenesis, but on the contrary, oral administration of a high concentration of dietary HE increased osteoclast numbers and promoted inflammation-induced alveolar bone loss. However, HE at 500 mg/kg can promote a bone-sparing effect on skeletal bone under physiological conditions.

Periodontitis stage and grade are associated with poor oral-health-related quality of life: Findings from the Porto Alegre cohort study.

AIM: To determine the association between periodontitis stage and grade with oral-health-related quality of life (OHRQoL). MATERIALS AND METHODS: This cohort was derived from the Porto Alegre study. The original sample was representative of more than 3 million inhabitants of a Brazilian urban area. Full-mouth periodontal examinations at six sites per tooth were performed at baseline and 5 years later. Periodontitis grade was determined by direct evidence of progression of attachment loss over the follow-up. Stage of periodontitis and OHRQoL, determined by the oral health impact profile version 14 (OHIP-14), were recorded at the follow-up examination. Mean ratios (MRs) and 95% confidence intervals (95% CIs) were estimated adjusting for age, sex, smoking, systemic diseases, tooth loss, and baseline periodontitis diagnosis. RESULTS: Five-hundred and ninety-nine individuals were analysed. Individuals with periodontitis grade C + stage II (MR = 1.49; 95% CI = 1.08-2.04) and stages III/IV (MR = 1.83; 95% CI = 1.25-2.66) had significantly higher OHIP scores than those without periodontitis or with periodontitis stage I/grade B. Individuals with periodontitis stages II and III/IV + grade B did not differ from those without periodontitis or with periodontitis stage I/grade B. CONCLUSION: Severity and progression rate of periodontitis are associated with poor OHRQoL.

Obesity as a risk factor for tooth loss over 5 years: A population-based cohort study.

AIM: To assess obesity as a risk factor for tooth loss over 5 years in an urban sample of Brazilian adults. MATERIALS AND METHODS: A total of 1586 individuals were surveyed using a multistage probabilistic approach. Five years later, 635 individuals 14-64 years old were re-examined. An incident case of tooth loss was determined for a participant that had lost at least one tooth over time. Obesity was evaluated by calculating body mass index at baseline and by the change in obesity status over time. RESULTS: Incident cases of tooth loss were significantly more frequent among obese (47.1%) than normal-weight individuals (32.4%) (p = .004). Obese individuals had 31% higher risk [relative risk (RR) =1.31; 95% confidence interval (95%CI) 1.04-1.65] for tooth loss than normal-weight individuals adjusting for age, socio-economic status, smoking, dental care and periodontitis. This association was significant for females (RR=1.47, 95%CI 1.08-2.01), but not for males. The risk for tooth loss was also modified by presence of periodontitis at baseline and lifetime smoking exposure. There was an increased risk for tooth loss for those that remained obese than those that remained normal weight. CONCLUSION: Obesity is associated with higher risk for tooth loss. This association was modified by sex, periodontal status and smoking.

Short-term effect of non-surgical periodontal treatment on local and systemic cytokine levels: Role of hyperglycemia.

BACKGROUND: The effect of non-surgical periodontal treatment on oral and systemic inflammatory mediators in subjects with periodontitis and hyperglycemia remains largely unknown. Therefore, the aim of this clinical study was to compare the short-term effect of non-surgical periodontal treatment on serum, saliva and GCF inflammatory markers levels in GP subjects with or without hyperglycemia. METHODS: Sixty subjects divided into four groups of equal size were selected to participate: type 2 diabetics with generalized periodontitis (T2DM + GP), pre-diabetics with GP (PD + GP), normoglycemic subjects with GP (NG + GP), and healthy controls. GCF, serum, and saliva samples were obtained at baseline and 30 days after scaling and root planning (SRP) and the levels of interleukin-1ß (IL-1 ß), IL-8, IL-6, IL-2, IL-5, IL-4, IL-10, Interferon gamma (IFN-γ), Granulocyte macrophage colony-stimulating factor (GM-CSF) and Tumor necrosis factor-alpha (TNF-α) were determined by ultrasensitive multiplex assay. Clinical periodontal measurements were recorded. RESULTS: SRP yielded significant improvement of all periodontal parameters for all GP groups (p < 0.01). A significant reduction in GCF levels of several cytokines were observed; however, only IL-1B and IFN-γ were consistently reduced post-treatment across all GP groups. Salivary levels of IL-1ß were significantly reduced in all GP groups following treatment. No significant differences were observed for serum levels after SRP. CONCLUSIONS: Periodontal treatment reduced local inflammatory markers, specifically IL-1B and IFN-γ, irrespective of the diabetes status. Periodontal treatment had no significant effect on serum levels of the inflammatory markers evaluated in this study.

Randomized clinical trials in periodontology: focus on outcomes selection

Abstract Randomized clinical trials (RCTs) are human studies carried out to compare different treatments or interventions, and their results are used to support clinical decision-making and improve patient care. Herein, the aim of this study was to review the selection process of study outcomes in periodontology. Primary outcomes should draw the main conclusions of the study, whereas secondary outcomes should only be used to help explain the main findings and generate future research hypothesis. Outcomes are classified as clinically relevant (CROs) or surrogate outcomes. CROs - the first option for primary outcome variables - should convey not only substantial health benefits, but also be deemed important by patients. In periodontology, tooth loss/retention and oral health-related quality of life (OHRQoL) are examples of CROs. While tooth loss has main limitations as a primary outcome, emerging evidence suggest that patient-reported outcome measures (PROMs) can accurately detect OHRQoL following periodontal therapy. When CROs cannot be assessed, validated surrogate outcomes can be used as proxies. Primary outcome variables should reflect a treatment endpoint at the patient level that can be easily used to inform decision-making in daily practice. These outcomes should allow the implementation of a treat-to-target concept in which the intervention can be clearly judged against a prespecified treatment target. Recently, the presence of at most 4 sites with periodontal probing depth ≥5 mm post-treatment was suggested as an effective endpoint for periodontal trials. In perspective, a combination of validated clinical parameters and PROMs will provide a more comprehensive assessment of periodontal treatments.

Prevalence and risk indicators of peri-implantitis after 8 to 10 years of function / Prevalência e indicadores de risco de peri-implantite após 8 a 10 anos em função

Abstract Introduction The investigation of peri-implant diseases risk indicators helps to prevent and target treatment techniques. Objective The aim of this cross-sectional study was to determine the occurrence of peri-implantitis and its potential risk indicator factors, besides to assess the long-term success and survival rates of dental implants after 8 to 10 years of function. Material and method For this, fifty individuals who had received their implant-supported rehabilitation between 2003 and 2005 were included. Data regarding demographics, medical and dental history were collected and a complete clinical examination was performed. Multivariate analysis was used to identify potential risk indicator factors related to the occurrence of peri-implantitis. Overall, 211 implants had been placed; 197 were in function, 9 were still submerged, and 5 had been lost. Result Success and survival rates were 81.5% and 97.6%, respectively. Peri-implant mucositis affected 77.1% of subjects and 52.3% of implants. Peri-implantitis was diagnosed in 14 individuals (29.2%) and 25 implants (12.7%). Subjects with osteoporosis (OR = 2.84) and generalized bleeding on probing (OR = 8.03) were significantly associated with higher odds of peri-implantitis. At the implant level, visible plaque (OR = 4.45) and deep probing depths (OR = 4.47) were significantly associated with peri-implantitis. Conclusion Through these results, our study suggests that osteoporosis and generalized periodontal/peri-implant mucosa inflammation increase the likelihood of peri-implantitis.

Resumo Introdução A investigação dos fatores indicadores de risco para as doenças peri-implantares auxilia na prevenção e direcionamento das técnicas de tratamento Objetivo O objetivo deste estudo transversal foi determinar a ocorrência de peri-implantite e seus potenciais fatores indicadores de risco, além de avaliar as taxas de sucesso e sobrevida em longo prazo dos implantes dentários após 8 a 10 anos de função Material e método Foram incluídos cinquenta indivíduos que receberam sua reabilitação implanto-suportada entre 2003 e 2005. Dados demográficos, história médica e odontológica foram coletados e um exame clínico completo foi realizado. A análise multivariada foi utilizada para identificar potenciais fatores indicadores de risco relacionados à ocorrência de peri-implantite. Ao todo, 211 implantes foram colocados; 197 estavam em função, 9 ainda estavam submersos e 5 haviam sido perdidos. Resultado As taxas de sucesso e sobrevivência foram de 81,5% e 97,6%, respectivamente. A mucosite peri-implantar afetou 77,1% dos indivíduos e 52,3% dos implantes. A peri-implantite foi diagnosticada em 14 indivíduos (29,2%) e 25 implantes (12,7%). Indivíduos com osteoporose (OR = 2,84) e sangramento generalizado à sondagem (OR = 8,03) foram significativamente associados a uma maior chance de peri-implantite. Ao nível do implante, a placa visível (OR = 4,45) e as maiores profundidades de sondagem (OR = 4,47) foram significativamente associadas à peri-implantite. Conclusão Por meio desses resultados, nosso estudo sugere que a osteoporose e a inflamação generalizada da mucosa periodontal / peri-implantar aumentam a probabilidade de peri-implantite.

The impact of maintenance on peri-implant health.

Most of the literature evaluating dental implants focuses on implant survival, which is a limited proxy for the successful rehabilitation of patients with missing teeth. Success should include not only survival but also lack of mechanical, biological, and esthetics problems. A comprehensive review of local and systemic risk factors prior to implant placement will allow the tailoring of treatment planning and maintenance protocols to the patient's profile in order to achieve longitudinal success of the therapy. This review discusses the role of controlling different risk factors and prevention/treatment of peri-implant mucositis in order to avoid peri-implantitis. Although the literature addressing the topic is still scarce, the existing evidence shows that performing optimal plaque control and regular visits to the dentist seem to be adequate to prevent peri-implant lesions. Due to impossibility of defining a probing depth associate with peri-implant health, radiographic evaluations may be considered in the daily practice. So far, there is a strong evidence linking a past history of periodontal disease to peri-implant lesions, but this is not so evident for other factors including smoking and diabetes. The prevention of biological complications starts even before implant placement and include a broader analysis of the patient risk profile and tailoring the rehabilitation and maintenance protocols accordingly. It should be highlighted that the installation of implants does not modify the patient profile, since it does not modify genetics, microbiology or behavioral habits of any individual.

Systemic Antibiotic Therapy Reduces Circulating Inflammatory Dendritic Cells and Treg-Th17 Plasticity in Periodontitis.

Periodontitis (PD) is a common dysbiotic inflammatory disease that leads to local bone deterioration and tooth loss. PD patients experience low-grade bacteremias with oral microbes implicated in the risk of heart disease, cancer, and kidney failure. Although Th17 effectors are vital to fighting infection, functional imbalance of Th17 effectors and regulatory T cells (Tregs) promote inflammatory diseases. In this study, we investigated, in a small pilot randomized clinical trial, whether expansion of inflammatory blood myeloid dendritic cells (DCs) and conversion of Tregs to Th17 cells could be modulated with antibiotics (AB) as part of initial therapy in PD patients. PD patients were randomly assigned to either 7 d of peroral metronidazole/amoxicillin AB treatment or no AB, along with standard care debridement and chlorhexidine mouthwash. 16s ribosomal RNA analysis of keystone pathogen Porphyromonas gingivalis and its consortium members Fusobacterium nucleatum and Streptococcus gordonii confirmed the presence of all three species in the reservoirs (subgingival pockets and blood DCs) of PD patients before treatment. Of the three species, P. gingivalis was reduced in both reservoirs 4-6 wk after therapy. Further, the frequency of CD1C+CCR6+ myeloid DCs and IL-1R1 expression on IL-17A+FOXP3+CD4+ T cells in PD patients were reduced to healthy control levels. The latter led to decreased IL-1ß-stimulated Treg plasticity in PD patients and improvement in clinical measures of PD. Overall, we identified an important, albeit short-term, beneficial role of AB therapy in reducing inflammatory DCs and Treg-Th17 plasticity in humans with PD.

The impact of maintenance on peri-implant health

Abstract Most of the literature evaluating dental implants focuses on implant survival, which is a limited proxy for the successful rehabilitation of patients with missing teeth. Success should include not only survival but also lack of mechanical, biological, and esthetics problems. A comprehensive review of local and systemic risk factors prior to implant placement will allow the tailoring of treatment planning and maintenance protocols to the patient's profile in order to achieve longitudinal success of the therapy. This review discusses the role of controlling different risk factors and prevention/treatment of peri-implant mucositis in order to avoid peri-implantitis. Although the literature addressing the topic is still scarce, the existing evidence shows that performing optimal plaque control and regular visits to the dentist seem to be adequate to prevent peri-implant lesions. Due to impossibility of defining a probing depth associate with peri-implant health, radiographic evaluations may be considered in the daily practice. So far, there is a strong evidence linking a past history of periodontal disease to peri-implant lesions, but this is not so evident for other factors including smoking and diabetes. The prevention of biological complications starts even before implant placement and include a broader analysis of the patient risk profile and tailoring the rehabilitation and maintenance protocols accordingly. It should be highlighted that the installation of implants does not modify the patient profile, since it does not modify genetics, microbiology or behavioral habits of any individual.

Obesity and dental caries among South Brazilian schoolchildren: a 2. 5-year longitudinal study

Abstract The aim of this study was to assess the association between weight status and ΔDMFS among 12-year-old schoolchildren from South Brazil. A total of 801 12-year-old schoolchildren were followed-up for 2.5 ± 0.3 years. Data collection included questionnaire, recording of anthropometric measures (height and weight), and caries examination. The outcome was the difference between DMFS (number of decayed, missing or filled surfaces) at follow-up and baseline (ΔDMFS). Weight status, based on body mass index-for-age Z-scores, was considered the main predictor variable. Negative binomial regression models were used to model the association, and rate ratios and their 95% confidence intervals were estimated. A multivariable fractional polynomial model was used to further explore the relationship between obesity and dental caries. DMFS increased by 0.86 (95%CI = 0.65-1.07), 0.91 (95%CI = 0.59-1.23), and 0.42 (95%CI = 0.03-0.80) for normal weight, overweight, and obese schoolchildren, respectively. Obese adolescents had significantly lower ΔDMFS than normal weight ones (p < 0.05). No significant association between categories of weight status and ΔDMFS was found (overweight, IRR=0.92, 95%CI = 0.69-1.21, p = 0.54; obese IRR = 0.75, 95%CI = 0.51-1.12, p = 0.16). However, the multivariable fractional polynomial model showed an inverted U shaped relationship with a decreasing ΔDMFS with increasing BMI (p < 0.05). This population-based longitudinal study showed an inverse association between obesity and ΔDMFS over a 2.5-year period among South Brazilian adolescents.

Oral Pathobiont Activates Anti-Apoptotic Pathway, Promoting both Immune Suppression and Oncogenic Cell Proliferation.

Chronic periodontitis (CP) is a microbial dysbiotic disease linked to increased risk of oral squamous cell carcinomas (OSCCs). To address the underlying mechanisms, mouse and human cell infection models and human biopsy samples were employed. We show that the 'keystone' pathogen Porphyromonas gingivalis, disrupts immune surveillance by generating myeloid-derived dendritic suppressor cells (MDDSCs) from monocytes. MDDSCs inhibit CTLs and induce FOXP3 + Tregs through an anti-apoptotic pathway. This pathway, involving pAKT1, pFOXO1, FOXP3, IDO1 and BIM, is activated in humans with CP and in mice orally infected with Mfa1 expressing P. gingivalis strains. Mechanistically, activation of this pathway, demonstrating FOXP3 as a direct FOXO1-target gene, was demonstrated by ChIP-assay in human CP gingiva. Expression of oncogenic but not tumor suppressor markers is consistent with tumor cell proliferation demonstrated in OSCC-P. gingivalis cocultures. Importantly, FimA + P. gingivalis strain MFI invades OSCCs, inducing inflammatory/angiogenic/oncogenic proteins stimulating OSCCs proliferation through CXCR4. Inhibition of CXCR4 abolished Pg-MFI-induced OSCCs proliferation and reduced expression of oncogenic proteins SDF-1/CXCR4, plus pAKT1-pFOXO1. Conclusively, P. gingivalis, through Mfa1 and FimA fimbriae, promotes immunosuppression and oncogenic cell proliferation, respectively, through a two-hit receptor-ligand process involving DC-SIGN+hi/CXCR4+hi, activating a pAKT+hipFOXO1+hiBIM-lowFOXP3+hi and IDO+hi- driven pathway, likely to impact the prognosis of oral cancers in patients with periodontitis.

Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations.

OBJECTIVES: This review proposes case definitions and diagnostic considerations of systemic disorders and conditions that affect the periodontal attachment apparatus. IMPORTANCE: Periodontal diseases and certain systemic disorders share similar genetic and/or environmental etiological factors, and affected patients may show manifestations of both diseases. Characterizing these diseases and the nature of the association between them could have important diagnostic value and therapeutic implications for patients. FINDINGS: Numerous systemic disorders and certain medications can affect the periodontal attachment apparatus and cause loss of periodontal attachment and alveolar bone. Although many of these disorders are rare or uncommon, they often cause significant loss of periodontal tissue by influencing periodontal inflammation or through mechanisms distinct from periodontitis. Most of these disorders are due to innate mechanisms and some are acquired via environmental factors or lifestyle. Several disorders affect periodontal inflammation through alterations in the host immune response to periodontal infection; others cause defects in the gingiva or periodontal connective tissue, instigate metabolic changes in the host that affect various tissues of the periodontal apparatus, or operate by other mechanisms. For some systemic disorders that are more common, their contribution to the loss of periodontal tissue is modest, while for others, contribution is not supported by clear evidence. Few systemic medications are associated with increased loss of periodontal tissue, and these are typically medications used in the treatment of malignancies. CONCLUSIONS: This review identifies systemic diseases and conditions that can affect the periodontal attachment apparatus and cause loss of periodontal supporting tissues and, where possible, presents case definitions for these. Many of these diseases are associated with a profound loss of periodontal attachment and alveolar bone, and for some of these disorders the periodontal manifestations may be among the first signs of the disease. These case definitions may be useful in the early diagnosis of these diseases and may contribute to an improvement in the management of periodontal manifestations and improve the quality of life for these patients.

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.

Manifestations of systemic diseases and conditions that affect the periodontal attachment apparatus: Case definitions and diagnostic considerations.

OBJECTIVES: This review proposes case definitions and diagnostic considerations of systemic disorders and conditions that affect the periodontal attachment apparatus. IMPORTANCE: Periodontal diseases and certain systemic disorders share similar genetic and/or environmental etiological factors, and affected patients may show manifestations of both diseases. Characterizing these diseases and the nature of the association between them could have important diagnostic value and therapeutic implications for patients. FINDINGS: Numerous systemic disorders and certain medications can affect the periodontal attachment apparatus and cause loss of periodontal attachment and alveolar bone. Although many of these disorders are rare or uncommon, they often cause significant loss of periodontal tissue by influencing periodontal inflammation or through mechanisms distinct from periodontitis. Most of these disorders are due to innate mechanisms and some are acquired via environmental factors or lifestyle. Several disorders affect periodontal inflammation through alterations in the host immune response to periodontal infection; others cause defects in the gingiva or periodontal connective tissue, instigate metabolic changes in the host that affect various tissues of the periodontal apparatus, or operate by other mechanisms. For some systemic disorders that are more common, their contribution to the loss of periodontal tissue is modest, while for others, contribution is not supported by clear evidence. Few systemic medications are associated with increased loss of periodontal tissue, and these are typically medications used in the treatment of malignancies. CONCLUSIONS: This review identifies systemic diseases and conditions that can affect the periodontal attachment apparatus and cause loss of periodontal supporting tissues and, where possible, presents case definitions for these. Many of these diseases are associated with a profound loss of periodontal attachment and alveolar bone, and for some of these disorders the periodontal manifestations may be among the first signs of the disease. These case definitions may be useful in the early diagnosis of these diseases and may contribute to an improvement in the management of periodontal manifestations and improve the quality of life for these patients.

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.

Screening of candidate biomaterials for alveolar augmentation using a critical-size rat calvaria defect model.

OBJECTIVE: To screen candidate biomaterials intended for alveolar augmentation relative to their potential to enhance local bone formation using a routine critical-size (ø8-mm) rat calvaria defect model. METHODS: One hundred and forty male Sprague Dawley outbred rats, age 11-12 weeks, weight 325-375 g, obtained from USDA approved breeder, randomised into 14 groups of 10 animals, each received one of the following treatments: sham-surgery (empty control), Bio-Oss (bovine HA/reference control), or candidate biomaterials including bovine HA, synthetic HA/ß-TCP and calcium phosphate constructs, mineralised/demineralised human bone preparations, a ß-TCP/calcium sulphate and an HA/calcium sulphate putty. A 4-week healing interval was chosen to discern local bone formation using incandescent and polarised light microscopy. Statistical analysis used one-way ANOVA followed by Bonferroni for pairwise comparisons. RESULTS: Candidate biomaterials all displayed biocompatibility. They exhibited limited, if any, appreciable bioerosion or biodegradation. No statistically significant differences in mean linear defect closure were observed among experimental groups, sham-surgery displaying the highest score (48.1 ± 24.3%). Sham-surgery also showed a significantly greater bone area fraction than all other groups (19.8 ± 13.9%, p < .001). The HA/calcium sulphate putty showed a significantly greater residual biomaterial area fraction than all other groups (61.1 ± 8.5%, p < .01). CONCLUSION: Within the limitations of this animal model, although biocompatible, none of the tested biomaterials enhanced local bone formation beyond the innate regenerative potential of this craniotomy defect.

Oral health related quality of life among pregnant women: a randomized controlled trial

Abstract: The aim of the present study was to compare negative impacts of oral conditions in Oral Heath Related Quality of Life (OHRQoL) assessed by the Oral Health Impact Profile-14 (OHIP-14) scores in pregnant women receiving or not comprehensive periodontal treatment. This randomized controlled clinical trial included pregnant women aged between 18 and 35 years old. Participants were randomized in a test group with 96 and a control group with 114 women. Patients in the test group received comprehensive periodontal treatment, supra and subgingival scaling and root-planning and periodontal maintenance appointments. The OHIP-14 was applied before and after treatment. The primary outcome was changes in OHIP-14 scores after follow-up period. The impact of having received or not comprehensive periodontal treatment on the change of the OHIP-14 scores was also investigated. Both groups showed significant reduction in OHIP-14 scores and effect size for the test group was 0.60 and 0.36 for the control group. Multinomial logistic regression analysis showed that participants of the control group had 5.9-fold odds (CI 95% 1.88-18.52) of worsening in OHIP-14 scores and their perception of oral conditions in relation to test group. Comprehensive periodontal treatment during pregnancy can reduce the negative impacts in OHRQoL.

Effect of Alcohol Consumption on Clinical Attachment Loss Progression in an Urban Population From South Brazil: A 5-Year Longitudinal Study.

BACKGROUND: The aim of this study is to investigate the impact of alcohol consumption on clinical attachment loss (AL) progression over a period of 5 years. METHODS: A multistage probability sampling strategy was used to draw a representative sample of the metropolitan area of Porto Alegre, Brazil. Five hundred thirty-two individuals (209 males and 293 females) aged 18 to 65 years at baseline with no medical history of diabetes and at least six teeth were included in this analysis. Full-mouth periodontal examinations with six sites per tooth were conducted at baseline and after 5 years. Alcohol consumption was assessed at baseline by asking participants about the usual number of drinks consumed in a week. Four categories of alcohol consumption were defined: 1) non-drinker; 2) ≤1 glass/week; 3) >1 glass/week and ≤1 glass/day; and 4) >1 glass/day. Individuals showing at least two teeth with proximal (clinical AL) progression ≥3 mm over 5 years were classified as having disease progression. Multiple Poisson regression models adjusted for age, sex, smoking, socioeconomic status, and body mass index were used to estimate relative risks (RRs) and 95% confidence intervals (CIs). RESULTS: Overall, individuals who consumed >1 glass/day had 30% higher risk for clinical AL progression (RR = 1.30; 95% CI: 1.07 to 1.58) than non-drinkers. Among males, risk of clinical AL progression for individuals drinking >1 glass/day was 34% higher than non-drinkers (RR = 1.34; 95% CI: 1.09 to 1.64). Never-smoker males drinking ≤1 glass/week had significantly lower risk for clinical AL progression than non-drinkers (RR = 0.52; 95% CI: 0.30 to 0.89), whereas those drinking >1 glass/day had significantly higher risk (RR = 1.50; 95% CI: 1.08 to 1.99). Among females, no association between alcohol consumption and clinical AL progression was observed. CONCLUSIONS: Alcohol consumption increased the risk of clinical AL progression, and this effect was more pronounced in males. Low dosages (≤1.37 g of alcohol/day) of alcohol consumption may be beneficial to prevent periodontal disease progression in males. The impact of alcohol cessation initiatives on periodontal health should be evaluated.