[A preliminary study on compliance of supportive treatment of patients with periodontitis after implant restoration therapy].

OBJECTIVE: To find out factors influencing the compliance of supportive treatment of patients with periodontitis who have received implant restoration therapy. METHODS: Patients who had completed periodontal and implant restoration treatment for more than 5 years in Department of Periodontology, Peking University Hospital of Stomatology were subjected to inclusion between March 2022 and August 2023.A questionnaire was compiled to gather the information including patients ' basic information (gender, age, and educational background etc.), smoking habits, general health conditions, oral hygiene habits, willingness to undertake periodontal and dental implant supportive treatment, actual fact on supportive treatment recorded in medical records, whether medical advices were correctly remembered, and reasons affected them to implement supportive therapy. The questionnaires were handed out to the above patients and filled during the process of follow-up treatment. Chi-square test, univariate and multivariate analysis of Logistic regression were employed to explore the correlations of these factors and the patients' compliance. RESULTS: In the study, 92 patients and questionnaires were collected and analyzed. The results indicated that oral hygiene habits and whether medical advices were correctly remembered had significant correlation with compliance (P < 0.05). Time constraint (47.0%) and difficulty in appointment registration (24.8%) were the top 2 reasons obstructed them to undertake supportive treatment. Although the vast majority of the patients indicated willingness to perform follow-ups, 55.4% of them wouldn't come back until the dentist called them back. The results of our study also indicated that the patients placed significantly less importance on the health of natural teeth than implants. CONCLUSION: In order to improve the compliance of supportive treatment, we suggest that dentists should put more emphasis on oral hygiene instruction, and knowledge regarding periodontitis should also be added as part of patient education contents. In the early stages of treatment, the patient should develop the habit of regular follow-up checks, More attention and patience should be given to elderly patients and those with lower level of education; use language that is easy to understand and printed medical instructions to help them remember. Patients can memorize better from refined doctors' advice, reinforcing care knowledge and refining medical advices can promote better follow-up treatment results. Motivating patients based on their characteristics is critical to improving compliance.

Duration and frequency of betel quid chewing affects periodontitis severity and life quality of people in Tanini Village, Kupang, Indonesia.

BACKGROUND: Chewing betel nuts can increase the risk of periodontal disease severity and potentially become malignant in the oral cavity. OBJECTIVE: This study aimed to investigate the effect of the duration and frequency of betel quid chewing behaviour on periodontitis severity and the life quality of people in Tanini Village, Kupang Regency, Indonesia. METHODS: The type of this study was an analytic observational study with a cross-sectional design. We used a questionnaire to obtain sociodemographic data. Oral Health Survey Basic Methods were used to measure debris index, plaque index, bleeding on probing, loss of attachment, and pocket depth. Behaviour and quality of life were measured by questionnaire and WHOQOL-BREF method as well. RESULTS: The largest number of respondents were male. Duration of chewing had a significant relationship with the frequency of chewing and periodontal status. Periodontitis was higher compared to all categories. The lifestyle of the community greatly influenced their behaviour in betel nut chewing and also affected the severity of their periodontitis and OHIs significantly. CONCLUSION: The lifestyle of betel nut chewing of the people in Tanini Village, greatly influences their behaviour. Prolonged and excessive use of betel nut induced significant adverse effects on human health. The longer and more often chew betel or areca nut, the higher the incidence of periodontitis, which significantly affects the quality of life as there is a possibility of the development of carcinogenesis, particularly in the oral cavity.

Mitochondrial Dysfunction in the Pathogenesis and Treatment of Oral Inflammatory Diseases.

Oral inflammatory diseases (OIDs) include many common diseases such as periodontitis and pulpitis. The causes of OIDs consist microorganism, trauma, occlusal factors, autoimmune dis-eases and radiation therapy. When treated unproperly, such diseases not only affect oral health but also pose threat to people's overall health condition. Therefore, identifying OIDs at an early stage and exploring new therapeutic strategies are important tasks for oral-related research. Mitochondria are crucial organelles for many cellular activities and disruptions of mitochondrial function not only affect cellular metabolism but also indirectly influence people's health and life span. Mitochondrial dysfunction has been implicated in many common polygenic diseases, including cardiovascular and neurodegenerative diseases. Recently, increasing evidence suggests that mitochondrial dysfunction plays a critical role in the development and progression of OIDs and its associated systemic diseases. In this review, we elucidated the critical insights into mitochondrial dysfunction and its involvement in the inflammatory responses in OIDs. We also summarized recent research progresses on the treatment of OIDs targeting mitochondrial dysfunction and discussed the underlying mechanisms.

Tratamento de periodontite estágio III localizado grau C em um indivíduo fumante: um relato de caso / Treatment of periodontitis stage III localized grade C in smoker individual: a case report

Objetivo: A periodontite é uma doença infecto-inflamatória que acomete os tecidos de inserção periodontal, e ser fumante representa um risco modificável significativo para todos os graus da doença. Ainda, indivíduos fumantes apresentam uma resposta inflamatória alterada quando comparados a não fumantes. Nesse contexto, o objetivo deste estudo foi reportar um relato de caso de tratamento periodontal de paciente fumante pesado. Relato de caso: O paciente DRS, sexo masculino, 22 anos, foi encaminhado à Faculdade de Odontologia da Universidade Federal de Pelotas (UFPel) com a queixa principal de necessidade de "realização de uma limpeza dentária". Na anamnese, relatou fumar 20 cigarros ao dia, há 7 anos (7 maços-ano). Na consulta inicial, foi encontrado índice de placa visível (IPV) de 100% e índice de sangramento gengival (ISG) de 66,67%. Foi encontrado cálculo supragengival como fator retentivo de placa (FRP) em 46,30% dos sítios. Estabeleceu-se o diagnóstico de periodontite estágio III localizado grau C. Os exames periodontais foram realizados por um único pesquisador calibrado e optou-se pelo tratamento periodontal não cirúrgico. Ao exame de 12 meses, o paciente apresentou IPV de 23,45% e ISG de 22,83%. Houve ausência de FRP. De uma forma geral, foi possível constatar a diminuição significativa das bolsas periodontais, bem como o ganho significativo de inserção clínica periodontal. Considerações finais: Dessa forma, é possível concluir a efetividade da terapia periodontal não cirúrgica, aliada à manutenção periodontal e instruções de higiene para o tratamento de periodontite estágio III, grau C, em paciente fumante.(AU)

Objective: Periodontitis is an infect-inflammatory diseases that affects the periodontal attachment tissues, and being smoker represents a significant modifiable risk for all degrees of the disease. Moreover, smokers have an altered inflammatory response when compared to non-smokers. Therefore, the aim of this study was to report a case report of periodontal treatment of a heavy smoker. Case report: A patient DRS, male, 22 years old, was referred to the School of Dentistry of the Federal University of Pelotas (UFPel) with the main complaint of the need to "perform a dental cleaning". During the anamnesis, he reported smoking 20 cigarettes a day for 7 years (7 pack-years). In the initial appointment, a visible plaque index (VPI) of 100% and a gingival bleeding index (GBI) of 66.67% were found. Supragingival calculus was found as a plaque retentive factor (PRF) in 46.30% of the sites. The diagnosis of periodontitis stage III localized grade C was established. Periodontal examinations were performed by a single calibrated researcher and non-surgical periodontal treatment was chosen. At the 12-month appointment, the patient had an VPI of 23.45% and an GBI of 22.83%. There was absence of PRF. In general, it was possible to observe a significant decrease in periodontal pockets, as well as a significant gain in periodontal clinical attachment. Final considerations: Thus, it is possible to conclude the effectiveness of non-surgical periodontal therapy, combined with periodontal maintenance and hygiene instructions for the treatment of periodontitis stage III localized grade C in a smoker.(AU)

Curcumin Attenuates Periodontal Injury via Inhibiting Ferroptosis of Ligature-Induced Periodontitis in Mice.

Periodontitis is a chronic infectious disease characterized by the destruction of connective tissue and alveolar bone that eventually leads to tooth loss. Ferroptosis is an iron-dependent regulated cell death and is involved in ligature-induced periodontitis in vivo. Studies have demonstrated that curcumin has a potential therapeutic effect on periodontitis, but the mechanism is still unclear. The purpose of this study was to investigate the protective effects of curcumin on alleviating ferroptosis in periodontitis. Ligature-induced periodontal-diseased mice were used to detect the protective effect of curcumin. The level of superoxide dismutase (SOD), malondialdehyde (MDA) and total glutathione (GSH) in gingiva and alveolar bone were assayed. Furthermore, the mRNA expression levels of acsl4, slc7a11, gpx4 and tfr1 were measured using qPCR and the protein expression of ACSL4, SLC7A11, GPX4 and TfR1 were investigated by Western blot and immunocytochemistry (IHC). Curcumin reduced the level of MDA and increased the level of GSH. Additionally, curcumin was proven to significantly increase the expression levels of SLC7A11 and GPX4 and inhibit the expression of ACSL4 and TfR1. In conclusion, curcumin plays a protective role by inhibiting ferroptosis in ligature-induced periodontal-diseased mice.

Pirfenidone Inhibits Alveolar Bone Loss in Ligature-Induced Periodontitis by Suppressing the NF-κB Signaling Pathway in Mice.

There has been increasing interest in adjunctive use of anti-inflammatory drugs to control periodontitis. This study was performed to examine the effects of pirfenidone (PFD) on alveolar bone loss in ligature-induced periodontitis in mice and identify the relevant mechanisms. Experimental periodontitis was established by ligating the unilateral maxillary second molar for 7 days in mice (n = 8 per group), and PFD was administered daily via intraperitoneal injection. The micro-computed tomography and histology analyses were performed to determine changes in the alveolar bone following the PFD administration. For in vitro analysis, bone marrow macrophages (BMMs) were isolated from mice and cultured with PFD in the presence of RANKL or LPS. The effectiveness of PFD on osteoclastogenesis, inflammatory cytokine expression, and NF-κB activation was determined with RT-PCR, Western blot, and immunofluorescence analyses. PFD treatment significantly inhibited the ligature-induced alveolar bone loss, with decreases in TRAP-positive osteoclasts and expression of inflammatory cytokines in mice. In cultured BMM cells, PFD also inhibited RANKL-induced osteoclast differentiation and LPS-induced proinflammatory cytokine (IL-1ß, IL-6, TNF-a) expression via suppressing the NF-κB signal pathway. These results suggest that PFD can suppress periodontitis progression by inhibiting osteoclastogenesis and inflammatory cytokine production via inhibiting the NF-κB signal pathway, and it may be a promising candidate for controlling periodontitis.

Chronic Periodontal Infection and Not Iatrogenic Interference Is the Trigger of Medication-Related Osteonecrosis of the Jaw: Insights from a Large Animal Study (PerioBRONJ Pig Model).

Background and Objectives: Antiresorptive drugs are widely used in osteology and oncology. An important adverse effect of these drugs is medication-induced osteonecrosis of the jaw (MRONJ). There is scientific uncertainty about the underlying pathomechanism of MRONJ. A promising theory suspects infectious stimuli and local acidification with adverse effects on osteoclastic activity as crucial steps of MRONJ etiology. Clinical evidence showing a direct association between MRONJ and oral infections, such as periodontitis, without preceding surgical interventions is limited. Large animal models investigating the relationship between periodontitis and MRONJ have not been implemented. It is unclear whether the presence of infectious processes without surgical manipulation can trigger MRONJ. The following research question was formulated: is there a link between chronic oral infectious processes (periodontitis) and the occurrence of MRONJ in the absence of oral surgical procedures? Materials and Methods: A minipig large animal model for bisphosphonate-related ONJ (BRONJ) using 16 Göttingen minipigs divided into 2 groups (intervention/control) was designed and implemented. The intervention group included animals receiving i.v. bisphosphonates (zoledronate, n = 8, 0.05 mg/kg/week: ZOL group). The control group received no antiresorptive drug (n = 8: NON-ZOL group). Periodontitis lesions were induced by established procedures after 3 months of pretreatment (for the maxilla: the creation of an artificial gingival crevice and placement of a periodontal silk suture; for the mandible: the placement of a periodontal silk suture only). The outcomes were evaluated clinically and radiologically for 3 months postoperatively. After euthanasia a detailed histological evaluation was performed. Results: Periodontitis lesions could be induced successfully in all animals (both ZOL and NON-ZOL animals). MRONJ lesions of various stages developed around all periodontitis induction sites in the ZOL animals. The presence of MRONJ and periodontitis was proven clinically, radiologically and histologically. Conclusions: The results of this study provide further evidence that the infectious processes without prior dentoalveolar surgical interventions can trigger MRONJ. Therefore, iatrogenic disruption of the oral mucosa cannot be the decisive step in the pathogenesis of MRONJ.

Perturbation of mitochondrial dynamics links to the aggravation of periodontitis by diabetes.

Diabetes and periodontitis are prevalent diseases that considerably impact global economy and diabetes is a major risk factor of periodontitis. Mitochondrial dynamic alterations are involved in many diseases including diabetes and this study aims to evaluate their relevance with diabetes aggravated periodontitis. Sixty mice are randomly divided into 4 groups: control, periodontitis, diabetes and diabetic periodontitis. Periodontitis severity is evaluated by alveolar bone loss, inflammation and oxidative stress status. Mitochondrial structural and functional defects are evaluated by the mitochondrial fission/fusion events, mitochondrial reactive oxygen species (ROS) accumulation, complex activities and adenosine triphosphate (ATP) production. Advanced glycation end product (AGE) and Porphyromonas gingivalis are closely related to periodontitis occurrence and development. Human gingival fibroblast cells (HGF-1) are used to investigate the AGE role and lipopolysaccharide (LPS) from Porphyromonas gingivalis (P-LPS) in aggravating diabetic periodontitis by mitochondrial dynamic and function alterations. In vivo, diabetic mice with periodontitis show severe bone loss, increased inflammation and oxidative stress accumulation. Among mice with periodontitis, diabetic mice show worse mitochondrial dynamic perturbations than lean mice, along with fusion protein levels inducing more mitochondrial fission in gingival tissue. In vitro, AGEs and P-LPS co-treatment causes severe.

The Role of Vitamin C and Vitamin D in the Pathogenesis and Therapy of Periodontitis-Narrative Review.

Periodontitis is a common disorder affecting the bone and soft tissues of the periodontal complex. When untreated, it may lead to severe mobility or even loss of teeth. The pathogenesis of periodontitis is complex, with crucial factors being chronic inflammation in gingival and periodontal tissues and oral microbiome alterations. However, recent studies highlight the alleged role of vitamins, such as vitamin C (VitC) and vitamin D (VitD), in the development of the disease. VitC regulates numerous biochemical reactions, but foremost, it is involved in synthesizing collagen. It was reported that VitC deficiency could lead to damage to the periodontal ligaments. VitC supplementation improves postoperative outcomes in patients with periodontitis. VitD is a steroid derivative that can be produced in the skin under ultraviolet radiation and later transformed into an active form in other tissues, such as the kidneys. VitD was established to decrease the expression of proinflammatory cytokines in gingiva and regulate the proper mineral density of teeth. Moreover, the supplementation of VitD was associated with better results in the nonsurgical treatment of periodontitis. In this review, we summarize recent knowledge on the role of vitamins C and D in the pathogenesis and treatment of periodontitis.

The mechanism of efferocytosis in the pathogenesis of periodontitis and its possible therapeutic strategies.

Periodontitis is an inflammatory disease characterized by the destruction of periodontal tissues, and its etiology is related to several systemic factors. At present, the destruction of periodontal tissues is considered to be the result of inflammation resolution disorders. Efferocytosis plays an important role in the resolution of inflammation, and defective efferocytosis is an essential factor in the persistence of many chronic inflammatory diseases. Therefore, this review will describe the mechanisms involved in the efferocytosis of macrophages in the pathogenesis of periodontitis and highlight emerging therapeutic strategies to provide new ideas for future periodontal treatment.

Onset of periodontitis - a registry-based cohort study.

OBJECTIVES: The present retrospective registry-based cohort study aimed to identify parameters associated with the onset of periodontitis in young adults. MATERIAL AND METHODS: A total of 345 Swedish subjects were clinically examined at age 19 years (as part of an epidemiological survey) and then followed up to 31 years through the Swedish Quality Registry for Caries and Periodontal diseases (SKaPa). The registry data including periodontal parameters were obtained for the period 2010-2018 (23-31 years). Logistic regression and survival models were used to identify risk factors for periodontitis (PPD ≥6 mm at ≥2 teeth). RESULTS: The incidence of periodontitis during the 12-year observation period was 9.8%. Cigarette smoking (modified pack-years; HR 2.35, 95%CI 1.34-4.13) and increased probing pocket depth (number of sites with PPD 4-5 mm; HR 1.04, 95%CI 1.01-1.07) at 19 years were risk factors for periodontitis in subsequent young adulthood. No statistically significant association was identified for gender, snuff use, plaque and marginal bleeding scores. CONCLUSION: Cigarette smoking and increased probing pocket depth (≥4 mm) in late adolescence (19 years) were relevant risk factors for periodontitis in young adulthood. CLINICAL RELEVANCE: Our study identified cigarette smoking and increased probing depth in late adolescence as relevant risk factors of periodontitis in young adulthood. Preventive programs should therefore consider both cigarette smoking and probing pocket depths in their risk assessment.

Income-related inequalities in the association of smoking with periodontitis: a cross-sectional analysis in Tokyo Metropolitan Districts.

OBJECTIVE: Socio-economic status (SES) and smoking are risk factors for periodontitis; however, their interaction has not been determined. We investigated the effect of modification of SES and smoking with periodontal conditions. MATERIALS AND METHODS: Data on the social background, smoking status, and dental examination of 1033 individuals residing in the Tokyo Metropolitan District were analyzed. The outcomes were the number of remaining teeth and the proportion of teeth with probing pocket depth (PPD) ≥ 4 mm and ≥ 6 mm. Multilevel linear and Poisson regression analyses were performed after adjusting for possible confounding factors, including SES, assessed by the average income of the residential area. RESULTS: The mean number of remaining teeth was 24.6 ± 4.8, and the proportion of teeth with PPD ≥ 4 mm and ≥ 6 mm was 31.2 ± 28.5% and 12.2 ± 18.1%, respectively. After adjusting for confounding factors, the lowest-income population had significantly lesser teeth (coefficient: - 0.46, 95% CI - 0.89, 0.02, p = 0.039) and a higher proportion of teeth with PPD ≥ 4 mm than the highest-income population (ratio of means: 1.22, 95% CI 1.03-1.44, p = 0.013). Significant interactions were observed; income inequalities in periodontitis were significant only among current smokers. CONCLUSION: Inequality in socio-economic status is associated with oral health inequalities. The adverse effects of smoking on periodontitis might be greater in the low-income population. CLINICAL RELEVANCE: The low-income population, especially current smokers, had significantly more compromised oral health than the high-income population. In addition to the emphasis on smoking cessation, the promotion of universal health coverage for dental care is necessary to reduce oral health inequalities.

Effect of Smoking Exposure on Nonsurgical Periodontal Therapy: 1-Year Follow-up.

This study investigated the influence of different levels of exposure to smoking on periodontal healing for 12 mo after nonsurgical periodontal therapy and supportive periodontal care every third month. Eighty smokers willing to quit smoking and with periodontitis were included. Participants were offered an individualized voluntary smoking cessation program. Data collection included questionnaires and a full-mouth periodontal examination. Group-based trajectory modeling was used to model smoking trajectories over the follow-up. The effect of smoking trajectory on periodontal parameters over time was estimated with mixed effects modeling. Three smoking patterns were identified: light smokers/quitters (n = 46), moderate smokers (n = 17), and heavy smokers (n = 17). For the periodontal data, the first factor, moderate periodontitis, included the number of sites with clinical attachment levels (CALs) of 4, 5, 6, and 7 mm; periodontal pocket depths (PPDs) of 4, 5, and 6 mm; and bleeding on probing. The second factor, severe periodontitis, consisted of the number of sites with a CAL ≥8 mm and PPD ≥7 mm. Heavy smokers commenced with a higher average CAL of 1.1 mm and 10 more sites with severe periodontitis than light smokers/quitters. While light smokers/quitters and moderate smokers obtained an average improvement of 0.6-mm PPD and 0.7-mm CAL, respectively, heavy smokers experienced 0.5-mm attachment loss. Heavy smokers had only a 50% reduction in the number of sites with moderate periodontitis when compared with light smokers/quitters and moderate smokers. While most participants benefited from nonsurgical periodontal therapy with results affected in a dose-response manner, the therapy had no effect on severe periodontitis among heavy smokers. Smoking cessation should be part of periodontal therapy; otherwise, limited benefits would be observed among heavy smokers, hindering the effect of treatment.

Tobacco smoke exacerbates Filifactor alocis pathogenicity.

AIM: Filifactor alocis has recently emerged as a periodontal pathobiont that appears to thrive in the oral cavity of smokers. We hypothesized that identification of smoke-responsive F. alocis genes would provide insight into adaptive strategies and that cigarette smoke would enhance F. alocis pathogenesis in vivo. MATERIALS AND METHODS: F. alocis was grown in vitro and cigarette smoke extract-responsive genes determined by RNAseq. Mice were exposed, or not, to mainstream 1R6F research cigarette smoke and infected with F. alocis, or not, in an acute ligature model of periodontitis. Key clinical, infectious, and immune data were collected. RESULTS: In culture, F. alocis growth was unaffected by smoke conditioning and only a small number of genes were specifically regulated by smoke exposure. Reduced murine mass, differences in F. alocis-cognizant antibody production, and altered immune profiles as well as altered alveolar bone loss were all attributable to smoke exposure and/or F. alocis infection in vivo. CONCLUSIONS: F. alocis is well-adapted to tobacco-rich conditions and its pathogenesis is enhanced by tobacco smoke exposure. A smoke-exposed ligature model of periodontitis shows promise as a tool with which to further unravel mechanisms underlying tobacco-enhanced, bacteria-induced disease.

Periodontitis Is Associated with Consumption of Processed and Ultra-Processed Foods: Findings from a Population-Based Study.

The association between periodontitis and lifestyle factors has been widely investigated. However, an association between periodontitis and dietary patterns has not been explored. Therefore, this study investigated the association between periodontitis and food consumption among a Southern Brazil population. Data from the 1982 Pelotas Birth Cohort were used (n = 537). The exposure, periodontitis, was clinically measured and classified using the AAP/CDC system, then two latent variables were defined: 'initial' and 'moderate/severe' periodontitis. The consumption of in natura, processed, and ultra-processed foods (NOVA classification) was the outcome and measured in calories using the food frequency questionnaire (FFQ). Confounders were sex, maternal education, smoking status, xerostomia, and halitosis. Data were analyzed by structural equation modeling. 'Initial' periodontitis was associated with a higher consumption of in natura food (standardized coefficient (SC) 0.102; p-value = 0.040), versus processed (SC 0.078; p-value = 0.129) and ultra-processed (SC 0.043; p-value = 0.400) foods. 'Moderate/severe' periodontitis was associated with higher consumption of ultra-processed foods (SC 0.108; p-value = 0.024), versus processed (SC 0.093; p-value = 0.053) and in natura (SC 0.014; p-value = 0.762) foods. 'Moderate/severe' periodontitis appears to be associated with the consumption of processed and ultra-processed foods.

Prevalence of Periodontitis among Patients Diagnosed with Marfan Syndrome: A Cross-Sectional Study Comparing Samples of Healthy Patients.

Periodontitis is an inflammatory condition caused by a bacterial plaque and characterized by progressive destruction of the tooth-supporting apparatus. Patients with Marfan syndrome (MFS) exhibit a connective tissue disorder, which can also affect oral soft and hard tissue. Thus, the aims of this cross-sectional study were to assess the association between periodontitis and MFS and secondly, to compare periodontal parameters and prevalence of disease with a control group (CG) without MFS. 152 patients (MFS = 76, CG = 76) were recruited to evaluate the following periodontal parameters: probing depth, gingival margin, clinical attachment level, plaque index, and bleeding on probing. The 2017 World Workshop guideline was followed for the diagnosis of the periodontal status. A multivariate analysis was performed using a multinomial logistic regression adjusted for age, gender, and smoking. The level of significance required was p < 0.05. Patients with MFS did not show a higher prevalence of periodontitis compared to the CG. However, patients with MFS did have higher values in probing depth, gingival recession, clinical attachment level, and plaque index compared to the CG patients (p < 0.05). In conclusion, although similar prevalence of periodontitis was found among the studied groups, MFS patients showed worse periodontal parameters.

Periodontal inflamed surface area in oral cavity associated with febrile neutropenia in patients with hematologic malignancy undergoing chemotherapy.

Febrile neutropenia (FN) is an infectious complication that develops during chemotherapy. Although the oral cavity can be an important infection route, it is unknown whether the oral environment is associated with FN. The present study examined the relationship between the oral environment using periodontal inflamed surface area (PISA), a new periodontal disease parameter, and FN in hematologic cancer patients undergoing chemotherapy. In this retrospective cohort study, 157 patients were divided into FN onset during chemotherapy (n = 75) and the FN negative groups (n = 82). The associations of risk factors related to the intraoral environment were assessed. Logistic regression analysis showed that types of blood cancer (odds ratio 1.98; P < 0.01), use of a high-risk regimen (odds ratio 4.44; P < 0.05), prophylaxis treatment with human granulocyte colony-stimulating factor (G-CSF) (odds ratio 4.15; P < 0.01) and PISA (odds ratio 1.02; P < 0.01) were independent factors associated with FN onset. Finally, propensity score matching was performed between two groups; 37 matched pairs were generated. PISA was significantly higher in the FN group than the FN negative group. There was a significant relationship between PISA and FN onset (P = 0.035). The present findings indicate that periodontitis treatment before starting cancer treatment is recommended as supportive care for preventing FN onset during chemotherapy.

Impact of Smoking Cessation on Periodontal Tissues.

There is cumulative evidence supporting the negative effects of smoking on periodontal tissues. Smoking cessation can be successfully accomplished through specific programs, including behaviour modification and medications, and has been suggested as a suitable way to reduce the risk of several diseases, including periodontitis. The aim of this review is to provide a concise overview of the current knowledge about the impact of smoking cessation on periodontal tissues and therapy, with data from studies published in the last 15 years. Literature was searched using Medline database from 2005 up to and including September 2020 using medical subject heading (MeSH) terms and other search terms, restricted to the English language. Studies were evaluated and summarised in a narrative review format. Results demonstrated that there is convincing evidence to support the benefits of tobacco cessation in reducing the risk of periodontitis and tooth loss. In addition, the harmful effects of smoking on periodontal tissues seem to be assuaged as the number of years since quitting increases. The existing current evidence, even limited, also shows that smoking cessation may result in additional benefits to the outcome of nonsurgical periodontal treatment. Periodontal care providers should not only check their patient's smoking habit for estimating risk of disease progression and predictability of periodontal therapy, but they should also help smokers improve their oral and systemic health by providing efficient and personalised tobacco-cessation counselling and treatment.

Estrés oxidativo en saliva generado por el humo de tabaco: impacto en la periodontitis y perspectivas hacia el uso de farmacología redox / Oxidative stress in saliva induced by tobacco smoke: impact on periodontitis and perspectives with redox pharmacology / Estresse oxidativo na saliva gerado pela fumaça do tabaco: impacto na periodontite e perspectivas para o uso da farmacologia redox

Numerosos reportes demuestran la presencia de biomarcadores de estrés oxidativo en la saliva de fumadores y hay un creciente interés en correlacionar estos procesos moleculares con la etiología de algunas enfermedades orales, como la periodontitis, una enfermedad inmunoinflamatoria crónica relacionada con un desequilibrio de la homeostasis redox celular. Objetivo: realizar una revisión narrativa sobre la relación entre la disminución de la capacidad antioxidante salival inducida por humo de tabaco, la periodontitis y el potencial uso de farmacología redox para el tratamiento de esta patología. Métodos: se realizó una búsqueda bibliográfica en bases de datos como PUBMED (NLM, NIH, NCBI) y SciELO. Resultados: existe evidencia que relaciona la baja capacidad antioxidante salival con un retraso en el restablecimiento de las condiciones normales en la cavidad oral ante el desarrollo de periodontitis. A su vez, el estado inflamatorio asociado colabora sinérgicamente, provocando un mayor daño tisular con pérdida de tejidos de soporte dentario, fenómeno que podría ser modulado por la acción de farmacología redox. Conclusiones: la intervención con farmacología redox, podría atenuar los biomarcadores de progresión de la enfermedad periodontal, constituyendo una herramienta prometedora para utilizar en conjunto con las estrategias de tratamiento tradicionales.

Numerous reports demonstrate the presence of oxidative stress biomarkers in the saliva of smokers and there is a growing interest in correlating these molecular processes with the etiology of some oral diseases, such as periodontitis, a chronic immunoinlammatory disease related to an imbalance of cellular redox homeostasis. Aims: achieve a narrative review on the relationship between the decrease in salivary antioxidant capacity induced by tobacco smoke, periodontitis, and the potential use of redox pharmacology for the treatment of this pathology. Methods: a bibliographic search was carried out in databases such as PUBMED (NLM, NIH, NCBI) and SciELO. Results: there is evidence that relates the low salivary antioxidant capacity with a delay in the reestablishment of normal conditions in the oral cavity before the development of periodontitis. In turn, the associated inflammatory state collaborates synergistically, causing greater tissue damage with loss of dental support tissues, a phenomenon that could be modulated by the action of redox pharmacology. Conclusions: intervention with redox pharmacology could attenuate the biomarkers of periodontal disease progression, constituting a promising tool to be used in conjunction with traditional treatment strategies.

Muitos artigos demonstram a presença de biomarcadores de estresse oxidativo na saliva de fumantes e há um interesse crescente em correlacionar esses processos moleculares com a etiologia de algumas doenças bucais, como a periodontite, uma doença imunoinlamatória crônica relacionada a um desequilíbrio da redox celular homeostase. Objetivo: realizar uma revisão narrativa sobre a relaçã o entre a diminuiçã o da capacidade antioxidante salivar induzida pela fumaça do tabaco, periodontite e o uso potencial da farmacologia redox para o tratamento desta patologia. Métodos: uma pesquisa bibliográica foi realizada usando bases de dados como PUBMED (NLM, NIH, NCBI) e SciELO. Resultados: há evidências que relacionam a baixa capacidade antioxidante salivar com o retardo no restabelecimento das condições normais da cavidade oral antes do desenvolvimento da periodontite. Por sua vez, o estado inflamatório associado colabora sinergicamente, causando maior dano tecidual com perda de tecidos de suporte dentário, fenômeno que poderia ser modulado pela açã o da farmacologia redox. Conclusões: a intervençã o com a farmacologia redox poderia atenuar os biomarcadores de progressã o da doença periodontal, constituindo-se em uma ferramenta promissora para ser utilizada em conjunto com estratégias tradicionais de tratamento.

A prospective interventional trial on the effect of periodontal treatment on Fusobacterium nucleatum abundance in patients with colorectal tumours.

Fusobacterium nucleatum is associated with the progression of colorectal cancer. Thus, the possibility of preventing colorectal cancer or its progression by targeting F. nucleatum has been explored. As F. nucleatum is associated with periodontitis, we analysed whether treating periodontitis could influence F. nucleatum abundance in the colon. Patients with colorectal tumours who underwent colonoscopy were recruited. Patients diagnosed with periodontitis by a dentist were treated for approximately 3 months. Endoscopic resection of colorectal tumours was performed after periodontitis treatment, and resected tumours were pathologically classified as high-(HGD) or low-grade dysplasia (LGD). Saliva and stool samples were collected before and after the treatment. Of the 58 patients with colorectal tumours, 31 were included in the study, 16 showed improvement in periodontitis, and 11 showed no improvement. Stool F. nucleatum levels before treatment were significantly lower in the LGD group than in the HGD group. A significant decrease in faecal F. nucleatum levels was observed in patients who underwent successful treatment but not in those whose treatment failed. Salivary F. nucleatum levels were not altered in patients despite periodontal treatment. Thus, successful periodontitis treatment reduces stool F. nucleatum levels and may aid research on periodontitis and suppression of colorectal cancer development.