Academic literature on the topic 'Periodontitis Longitudinal studies'

Abstract Aims This systematic review aimed to estimate the effect of tobacco smoking cessation on the risk for periodontitis compared to the risk among never-smokers and to evaluate the effect of tobacco smoking cessation on the clinical outcomes of nonsurgical periodontal treatment. Methods Electronic searches were performed in PubMed, Scopus, and Embase. Search strategy included MeSH and free terms: periodontitis, periodontal diseases, smoking, tobacco use, tobacco, tobacco products, cigarette, pipe, and cigar. Only original prospective longitudinal observational and interventional studies that investigated the association between smoking cessation and periodontitis onset or progression were included. Meta-analyses were conducted to summarize the evidence. Results A total of 2743 articles were identified in electronic searches; out of which only six were included in the meta-analysis. Pooled estimates showed that the risk of periodontitis incidence or progression among those who quit smoking was not significantly different from the risk for never-smokers (risk ratio [RR] = 0.97; 95% confidence interval [CI] = 0.87% to 1.08%). Smokers had approximately 80% higher risk of periodontitis than quitters (RR = 1.79; 95% CI = 1.36% to 2.35%) and never-smokers (RR = 1.82; 95% CI = 1.43% to 2.31%). Periodontal therapy resulted in up to 0.2 mm (95% CI = −0.32% to −0.08%) higher gain in attachment level and extra 0.32 mm (95% CI = 0.07% to 0.52%) reduction in pocket depth among quitters over nonquitters after short follow-up (12–24 months). Conclusions Few studies on the topic were identified. Smoking cessation reduced the risk for periodontitis onset and progression, and improved the outcomes of nonsurgical periodontal therapy. Implications This review provides the first quantitative evidence of the impact of smoking cessation on the risk for periodontitis onset and progression. The findings have demonstrated that the risk for periodontitis becomes comparable to that of never-smokers and that nonsurgical periodontal treatment outcomes improve after smoking cessation. Dental professionals ought to consider smoking cessation interventions as a relevant component of the periodontal therapy.

Background: The study aimed to estimate and compare the incidence and progression of chronic periodontitis among two generations of older Australian adults. Methods: Data were from two population-based cohort studies of Australian older adults aged 60+ years South Australian Dental Longitudinal Studies (SADLS), SADLS I (1991–1992) and SADLS II (2013–2014). American Academy of Periodontology/the U.S. Centres for Disease Control and Prevention (CDC/AAP), and the 2018 European Federation of Periodontology classification (EFP/AAP) case definitions were used to define and calculate the incidence and progression of chronic periodontitis. Multivariable Poisson regression models were used to estimate incidence risk ratios (IRRs) of periodontitis. Results: A total 567 and 201 dentate respondents had periodontal exams in SADLS I and II, respectively. The incidence rate was greater in SADLS II than in SADLS I, approximately 200 vs. 100/1000 person years, respectively. Current smokers had more than two times higher IRRs, 2.38 (1.30–4.34) and 2.30 (1.24–4.26), than their non-smoking counterparts in the previous generation under the CDC/AAP and EFP/AAP, respectively. Conclusions: The most recent generation of older adults has greater incidence and progression of periodontitis than the previous generation. Being a current tobacco smoker was a significant risk factor for both the incidence and progression of periodontitis.

The biologically active form of vitamin D, 1,25 dihydroxyvitamin D (1,25(OH)2D) and its receptor, the vitamin D receptor (VDR), play roles in maintaining oral immunity and the integrity of the periodontium. Results of observational cross-sectional clinical studies investigating the association between vitamin D serum level and the incidence and severity of chronic periodontitis indicate that, perhaps owing to the immunomodulatory, anti-inflammatory, and antibacterial properties of 1,25(OH)2D/VDR signalling, a sufficient serum level of vitamin D is necessary for the maintenance of periodontal health. In cases of established chronic periodontitis, vitamin D supplementation is associated with reduction in the severity of periodontitis. As cross-sectional studies provide only weak evidence for any causal association and therefore are of questionable value, either longitudinal cohort studies, case controlled studies, or randomized control trials are needed to determine whether or not deficiency of vitamin D is a risk factor for chronic periodontitis, and whether or not vitamin D supplementation adjunctive to standard periodontal treatment is in any way beneficial. In this article, we discuss the relationship between vitamin D, oral immunity and periodontal disease and review the rationale for using vitamin D supplementation to help maintain periodontal health and as an adjunct to standard periodontal treatment.

Background: The likelihood of experiencing the impact of chronic disease rises with age, and cumulative functional deficits over time increase the risk of frailty in older adults. The exact causes of frailty are not clear, and research is needed to identify appropriate intervention measures to reduce risk of developing frailty in old age. Objective: To review the evidence on the relationship between frailty, dental status and chronic periodontitis and to determine if improvements in oral health of older adults can contribute to reversal of frailty. Results: The oral cavity is the entry point to the gastro-intestinal tract, and natural teeth facilitate efficient mastication of food prior to swallowing and subsequent digestion. The loss of natural teeth, which is gradual and cumulative over the life course, is associated with diminished nutritional intake, especially in older adults. Furthermore, chronic periodontitis has been postulated as a risk factor for frailty. The evidence supporting a strong relationship between oral health status and frailty is not clearcut. Cross sectional studies suggest an association with missing teeth and chronic periodontal inflammation. However, there are very few longitudinal studies and accordingly, it is not currently possible to claim a causal relationship. As yet, there is no evidence to suggest that improvements in oral health contribute to reversal of frailty. Conclusion: Longitudinal studies with robust designs are required to better inform the relationship across functional dentition, chronic periodontitis and frailty in older adults.

There is accumulating data suggesting that periodontitis is associated with increased risk of systemic and autoimmune diseases, including cardiovascular disease, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE), and there is an unmet need to identify these individuals early. With the periodontal bacteria Porphyromonas gingivalis (Pg) as one of the key drivers of periodontitis, we set out to investigate whether antibodies to Pg virulence factor arginine gingipain (Rgp) could serve as a biomarker for periodontitis patients at increased risk of autoimmunity and systemic disease. We measured serum anti-Rgp IgG in three study populations: PAROKRANK (779 individuals with myocardial infarction (MI); 719 controls), where 557 had periodontitis, and 312 were positive for autoantibodies associated with RA/SLE; the PerioGene North pilot (41 periodontitis; 39 controls); and an SLE case/control study (101 SLE; 100 controls). Anti-Rgp IgG levels were increased in severe periodontitis compared to controls (p < 0.0001), in individuals positive for anti-citrullinated protein antibodies (p = 0.04) and anti-dsDNA antibodies (p = 0.035), compared to autoantibody-negative individuals; and in MI patients versus matched controls (p = 0.035). Our data support longitudinal studies addressing the role of anti-Rgp antibodies as biomarkers for periodontitis patients at increased risk of developing autoimmunity linked to RA and SLE, and mechanisms underpinning these associations.

Purpose.Inflammation and tissue breakdown are led by an array of inflammatory destructive mediators associated with initiation and progression of inflammatory diseases like periodontitis. Current evidence shows that these inflammatory mediators have a definitive role in the pathogenesis of various systemic diseases with an inflammatory component. Interleukin-21 (IL-21) has been associated with systemic diseases like rheumatoid arthritis and Crohn’s disease that follow a chronic inflammatory cascade. Similarly recent studies have associated Interleukin-21 levels with periodontitis. This systematic review was aimed to assess the levels of IL-21 in subjects with periodontitis.Methods.A complete literature search was done in PubMed, Medline, Science Direct, and Cochrane databases and Google Scholar based on the inclusion/exclusion criteria. Six relevant articles were procured. Full text was read individually by two reviewers and data extraction was done based on STROBE statement.Results.After data extraction five observational and one interventional study were obtained. All the studies showed an increased expression of IL-21 in periodontitis and the interventional study showed reduction in IL-21 levels after nonsurgical periodontal therapy (NSP).Conclusion.Interleukin-21 levels are higher in periodontitis than controls. With this limited evidence further longitudinal studies are required to consider this as a definitive inflammatory marker.

ABSTRACT Introduction: It is possible that physical activity protects the periodontium by mitigating excessive inflammatory response of the individual. There is some evidence from longitudinal studies and a prospective study demonstrating that physically active adults have experienced a decrease in the risk of periodontitis. To date no study has jointly explored the relationship of physical activity and periodontitis using inflammatory biomarkers. Objective: In this regard, the objective was to assess the bone tissue behavior of rats with experimental periodontitis subjected to aquatic exercise. Methods: Twenty-four male Wistar rats were divided into four groups: 1) without periodontitis and without exercise (CS); 2) without periodontitis and with exercise (CE); 3) with periodontitis and without exercise (DPS); 4) with periodontitis and with exercise (DPE). The animals from groups CE and DPE had swimming sessions for four weeks and the DPS and DPE groups were subjected to ligature-induced periodontitis. After 30 days the animals were sacrificed, and had their right and left hemimandibles removed for radiographic and histological analysis. The data obtained were analyzed and evaluated through ANOVA and Tukey tests. Results: Bone loss in the animals from the DPE group was found to be significantly lower (61.7 ± 2.2; p <0.05) than in those from the DPS group (84.5 ± 1.2; p <0.05), while in terms of the number of osteoblasts (DPS=11.0 ± 1.4; DPE=10.7 ± 5.2) and osteocytes (DPS=17.3 ± 3.1; DPE=19.0 ± 4.4), there was no significant decrease (p <0.05) in the groups subjected to experimental periodontitis, regardless of physical exercise. Conclusion: Physical exercise was found to have a protective effect in relation to bone height and did not influence bone density. Level of evidence II; Therapeutic studies - investigation of treatment results.

Abstract Increasing evidence suggests that there is a linkage between cognitive function and oral health. However, there are few systematic reviews with meta-analysis have been conducted to evaluate the strength of this association. Moreover, existing studies usually focused on unidirectional associations between cognitive function and oral health; no research has demonstrated this inter-relationship in a longitudinal study. This study aims to systematically assess the magnitude of the bidirectional association between oral health and cognitive decline for studies using longitudinal data. Six international databases were searched up until December 31, 2019. Random-effects pooled Risk Ratios (RRs) with 95% confidence intervals (CIs) were calculated. The grading of recommendations assessment, development, and evaluation (GRADE) system was used to assess the quality of evidence. From 13,251 potentially eligible articles, 54 longitudinal studies were included in the systematic review and 18 were in meta-analysis. Meta-analysis was performed for tooth loss and periodontitis disease. Random effects analysis showed, with statistically low heterogeneity, Risks of cognitive decline included suboptimal dentition (&lt;20 teeth) (RR 1.44, 95% CI 1.03-3.65) and periodontitis diseases (RR 1.48, 95% CI 1.22-1.81). Cognitive decline was a risk factor for tooth loss (RR 1.54, 95% CI 1.23-9.69). The overall quality of evidence, however, was rated as very low. The result of this review highlights that cognitive decline is a risk factor for poor oral health, and older adults with suboptimal oral health appear to have an increased risk of cognitive impairment. More studies with rigorous designs are needed to further examine this association.

This study aimed to explore the association between pre-pregnancy BMI and longitudinal changes in inflammatory markers from the second trimester of pregnancy to 6–8 weeks postpartum in women with periodontitis. This is a secondary exploratory analysis of 68 women who took part in a feasibility clinical trial in Rio de Janeiro, Brazil. Inflammatory markers included C-reactive protein (CRP), interleukin-6 (IL-6), interleukin-10 (IL-10), and matrix metalloproteinase-9 (MMP-9) blood concentrations at 11–22 (T0) and 30–36 gestational weeks (T1), and 6–8 weeks postpartum (T3). Longitudinal generalised linear mixed-effects models were used to identify possible associations between pre-pregnancy BMI and changes in concentrations of inflammatory markers. Pre-pregnancy excess weight (β = 4.39; 95% CI, 2.12–6.65) was significantly associated with increased CRP levels from pregnancy to postpartum. There were no significant associations between pre-pregnancy BMI and longitudinal changes in IL-6, IL-10 and MMP-9. Our findings provide evidence that a higher pre-pregnancy BMI may lead to increases in CRP levels during pregnancy in women with periodontitis, irrespective of the severity of clinical periodontal parameters. Further studies need to investigate if predictors of changes in inflammatory markers can be used as prognostic factors for gestational outcomes.

There is a debate over the association between low testosterone levels in body fluids and the occurrence of chronic periodontitis (CP). The aim of the present systematic review was to assess whether low testosterone levels in body fluids reflect CP. In order to identify studies relevant to the focus question: “Is there a relationship between low testosterone levels in body fluids and CP?” an electronic search without time or language restrictions was conducted up to June 2016 in indexed databases using different keywords: periodontitis, chronic periodontitis, periodontal diseases, testosterone, and gonadal steroid hormones. A total of eight studies were included in the present systematic review. The number of study participants ranged from 24 to 1,838 male individuals with ages ranging from 15 to 95 years. Seven studies measured testosterone levels in serum, two studies in saliva, and one study in gingiva. Four studies reported a negative association between serum testosterone levels and CP. Two studies reported a positive association between decreased testosterone levels in serum and CP. Increased levels of salivary testosterone among patients with CP were reported in one study; whereas one study reported no significant difference in the concentration of salivary testosterone between patients with and without CP. One study identified significant increase in the metabolism of testosterone in the gingiva of patients with CP. Within the limits of the evidence available, the relationship between low testosterone levels and CP remains debatable and further longitudinal studies and control trials are needed.

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Periodontal diseases are the result of complex interrelationships between bacterial biofilm and factors related to the host response. These relationships can be modified by several factors, among them the smoke. Many studies support the evidence that the smoke has a detrimental effect on the health of the periodontium. However, the effect of this habit in the results of periodontal treatment is still controversial and longitudinal studies of smokers and never smokers undergoing periodontal therapy are needed. Initially, 14 never smokers and 11 smokers completed the non-surgical periodontal treatment. After examination of three months, three participants were lost: one from the first group and two from the second. Thus, this study aimed to evaluate the response of 13 never smokers and nine smokers with chronic periodontitis, 12 months after this therapeutic approach. This study aimed to evaluate the response to non-surgical periodontal therapy in smokers and never smokers with chronic periodontitis, after a period of 12 months. Patients in both groups who received non-surgical periodontal treatment, were analyzed with respect to changes in bleeding on probing (BoP, BoP1 and BoP2), probing depth (PD), clinical attachment level (CAL), visible plaque index (VPI) and gingival bleeding index (GBI). To evaluate these parameters, trained and calibrated examiners performed periodontal clinical examinations prior to periodontal therapy and three, six and 12 months after treatment completion. The changes in scores for bleeding on probing were considered primary outcome and changes in other clinical parameters were secondary outcomes. The response to non-surgical periodontal therapy was similar between smokers and never smokers in changes related to VPI, mean and different strata of PD, BoP and BoP2. Similarities were also observed in BoP, BoP 1 and BoP 2 in different strata of PD, except for BoP 1 on PD 1-3mm in ever smokers had greater reductions. Differences between groups were also observed in the presence of GBI and BoP1. Changes in CAL were higher in the group of never smokers, the statistic difference being borderline.
As doenças periodontais são resultantes de inter-relações complexas entre biofilme bacteriano e fatores relacionados à resposta do hospedeiro. Essas relações podem ser modificadas por vários fatores, dentre eles, o fumo. Muitos estudos suportam a evidência de que o fumo prejudica a saúde do periodonto. Porém, o efeito desse hábito nos resultados do tratamento periodontal ainda é controverso e estudos de acompanhamento longitudinal de fumantes e nunca fumantes submetidos à terapia periodontal são necessários. Inicialmente, 14 nunca fumantes e 11 fumantes completaram o tratamento periodontal não cirúrgico. Após o exame de três meses, foram perdidos três participantes: um do primeiro grupo e dois do segundo. Assim, esse trabalho objetivou avaliar a resposta de 13 nunca fumantes e nove fumantes com periodontite crônica, 12 meses decorridos do término dessa abordagem terapêutica. Pacientes de ambos os grupos que receberam tratamento periodontal não cirúrgico, foram analisados com relação a alterações no sangramento à sondagem (SS, SS1 e SS2), na profundidade de sondagem (PS), no nível de inserção clínica (NIC) e nos índices de placa visível (IPV) e de sangramento gengival (ISG). Para a avaliação desses parâmetros, examinadores treinados e calibrados realizaram exames clínicos periodontais previamente à terapia periodontal e três, seis e 12 meses após o tratamento concluído. As mudanças nos escores de sangramento à sondagem foram consideradas desfecho primário e as alterações nos demais parâmetros clínicos avaliados, os desfechos secundários. A resposta à terapia periodontal não cirúrgica foi semelhante entre fumantes e nunca fumantes em relação às alterações de IPV, médias e diferentes estratos de PS, SS e SS2. Semelhanças também foram observadas em SS, SS1 e SS2 nos diferentes estratos de PS, com exceção de SS1 em PS de 1-3mm em que nunca fumantes tiveram maiores reduções. Diferenças entre os grupos também foram observadas no ISG e na presença de SS1. As alterações no NIC foram maiores no grupo de nunca fumantes, sendo a diferença estatística borderline.

O objetivo desta tese foi estimar a progressão de perda de inserção periodontal (PI) após 5 anos de acompanhamento e estudar fatores de risco para a sua ocorrência em uma amostra urbana do sul do Brasil. O Estudo de Porto Alegre teve início em 2001 com a constituição de uma amostra representativa da região metropolitana obtida por uma amostragem probabilística proporcional estratificada de múltiplo-estágio. A amostra inicial constituiu-se de 1465 indivíduos dentados e 121 desdentados (14-103 anos de idade; média 37,9 anos, desvio padrão 13,3). Em 2006, 697 (47,6%) indivíduos dentados (294 homens e 403 mulheres) e 48 desdentados participaram novamente. Dados demográficos, comportamentais e socioeconômicos foram coletados através de um questionário estruturado. PI foi obtida em seis sítios de todos dentes, por periodontistas calibrados. Duas análises foram realizadas, uma para estimar a ocorrência da progressão de PI proximal, e outra para estimar a associação de fatores de risco para progressão de PI. Do total, 56,0% e 36,2% dos indivíduos apresentaram progressão de PI ≥3mm em 2+ e 4+ dentes, respectivamente. Em geral, a extensão da progressão foi localizada, com média de 3,76 dentes com progressão ≥3mm. A média de progressão de PI foi 0,3mm/ano, sendo que 67% dos indivíduos apresentaram taxa de progressão moderada (>0,1mm/ano a ≤0,5mm/ano), 16,9% leve/nenhuma progressão (≤0,1mm/ano) e 16,1% rápida progressão (>0,5mm/ano). A progressão de PI aumentou estatisticamente com a idade e foi significativamente maior nos homens. Na análise multivariável pode-se observar que: indivíduos de 30-49 e 50+ anos tiveram risco duas vezes maior do que indivíduos com <30 anos; baixa educação aumentou o risco de progressão em 53%; homens nunca-fumantes tiveram risco aumentado em 33% comparados a mulheres nunca-fumantes; entre os fumantes, o risco aumentou em 8% para homens e em 21% para mulheres a cada 10 maços-ano. Pode-se concluir que uma grande proporção desta amostra urbana brasileira apresentou progressão de PI. Idade, gênero, educação e fumo foram encontrados como fatores de risco independentes para progressão de PI. Medidas de promoção de saúde devem ser estabelecidas para diminuir a ocorrência e progressão das doenças periodontais destrutivas nessa população.
The aim of this thesis was to estimate the occurrence of progression of periodontal attachment loss (PAL) and determine its risk factors in an urban sample from South Brazil. The “Porto Alegre Study” started in 2001 and was an epidemiological survey with a representative sample of the Porto Alegre metropolitan area obtained by a multistage probability sampling. At baseline, the sample comprised 1465 dentate and 121 edentulous individuals (mean age: 37.9 years, standard deviation:13.3). After 5 years, 697 (47.6%) dentate (294 males and 403 females) and 48 edentulous subjects were re-evaluated. Demographics, behavioral and socioeconomic data were collected using a structured questionnaire. PAL was obtained in six sites of all teeth present by calibrated periodontists. Two analyses were performed, one aiming at estimating the occurrence of PAL progression, and another aiming at determining risk factors for PAL progression. Overall, 56.0% and 36.2% of the subjects presented PAL progression ≥3mm in 2+ and 4+ teeth, respectively. In general, extent of progression was localized with 3.76 teeth presenting PAL progression ≥3mm. Overall mean PAL progression was 0.3mm/year. When subjects were categorized according to the mean annual PAL progression, 67.0% of subjects showed a moderate progression rate (>0.1mm/year to ≤0.5mm/year), whereas 16.1% were deemed as having no/ slight (≤0.1mm/year) and 16.9% as rapid progression (>0.5mm/year) rates. PAL progression increased significantly with age and was statistically higher among males. The multivariable model showed that: 30-49 and 50+ years-old individuals had approximately two times higher risk than <30 year-olds; low education increased the risk of PAL progression by 53%; among never-smokers, males were 33% more likely to experience PAL progression than females, while the risk increased by 8% for smoker males and by 21% for smoker females per 10 packyears of lifetime smoking exposure. It can be concluded that a large proportion of this urban Brazilian sample was affected by PAL progression underscoring the need for health promotion initiatives aiming at preventing progression of destructive periodontal disease. Age, gender, education and smoking were found to be independent risk factors for PAL progression.

I Sverige finns en hög frekvens av rotfyllda tänder med apikal parodontit och en praxis för behandling saknas. Denna studie syftar till att röntgenologiskt kartlägga progressionen av apikal parodontit vid rotfyllda tänder som ej blivit föremål för ytterligare endodontisk eller kirurgisk behandling och att identifiera variabler som påverkar progressionen för att ge ett bättre underlag för behandlingsbeslut. Röntgenbilder på rotfyllda tänder med apikal parodontit som lämnats utan åtgärd (n = 120) granskades avseende förändringen av den apikala parodontiten under minst en 3-års period under åren 2002-2011. Progression av den apikala parodontiten observerades i 22,5% av de studerade tänderna, trots att man sannolikt tidigare bedömt att den apika parodontiten inte behövde behandling eller att man kunde avvakta med behandling. Ingen av de studerade variablerna: den ursprungliga apikala parodontitens storlek, rotfyllningens längd, rotfyllningens täthet, typ av koronal restaurering eller den koronala restaureringens täthet befanns ha något samband med den apikal parodontitens progression. Oförändrad apikal parodontit observerades vid 50 % av tänderna och signifikant oftare i överkäken (p=0.02).
There is a high frequency of endodontically treated teeth with apical periodontitis in Sweden, but a lack of a well-established practice of how to deal with these. This study aims to investigate radiographic progression of untreated apical periodontitis in previously root-filled teeth left without intervention and to identify factors that affect the progression in order to reach a better foundation for making treatment decisions. Radiographs of root-filled teeth with apical periodontitis (n = 120) were examined with regards to the change of the apical periodontitis over at least three years during 2002-2011.Progression of the apical periodontitis was observed in 22.5 % of the studied teeth in spite of probable clinical decisions that treatment was not needed for the apical periodontitis or treatment could be postponed. None of the studied variables: the size of the apical periodontitis, the length of the root-filling, the sealing quality of the root-filling, the type of the coronal restoration or the sealing quality of the coronal restoration were found to be correlated to the progression of the apical periodontitis. The apical periodontitis was unchanged in 50 % of the teeth and observed more often in the maxilla (p=0.02).

Background: Oral infections are prevalent in the adult population. Their impact includes the implication as a risk factor for Alzheimer’s disease (AD), altering its progression. One of the potential mechanisms involves immune mediators such as circulating cytokines. Objective: The goal of the present study was to investigate the prevalence of oral infections and blood levels of IL-1β, TNF-α, and IL-6 in patients with AD, mild cognitive impairment (MCI), and controls. Methods: Sixty-five elderly were evaluated (25 AD, 19 MCI, and 21 controls) by the following methods: Mini Mental State Exam, Questionnaire of Functional Activities, periodontal and oral evaluation, and blood concentrations of IL-1β, TNF-α and IL-6. Results: Patients with AD had high serum IL-6 levels (p = 0.029), and patients with periodontitis had high serum TNF-α levels (p = 0.005). There was an association between IL-6 and TNF-α in patients with AD/MCI and periodontitis (p = 0.023). Conclusion: The increased levels of TNF-α and IL-6 in this study suggests their implication in the overlapping mechanisms between oral infections and AD. Longitudinal studies are necessary for further investigation.