Review of The Association between Obesity and Periodontitis among adults

Abstract

1 Review of The Association between Obesity and Periodontitis among adults Nazeeha Hakami Thesis submitted in partial fulfilment of the requirements for the degree of Master of Science in Dental Public Health 2025 Institute of Epidemiology & Health Care Faculty of Population Health Sciences KVYK4 2 Acknowledgments: I would like to express my sincere gratitude to my supervisor, Prof. Georgios Tsakos, for his guidance, patience, and invaluable feedback throughout this dissertation. His continuous encouragement and expertise have been fundamental in shaping my work and enabling me to complete this study. I am also thankful to the faculty and staff of the MSc Dental Public Health programme at UCL for their support and dedication, which created a stimulating and supportive academic environment. Most importantly, I extend my deepest gratitude to my family for their unwavering love and support throughout this journey. I dedicate this work to my late father, whose encouragement and belief in me have been a constant source of strength. Though he passed away before I completed this programme, his memory has been an enduring inspiration and motivation to persevere. 3 Abstract: Background: Obesity and periodontitis are two highly prevalent chronic conditions that share several behavioural, biological, and socio-economic determinants. Obesity has been implicated in systemic inflammation and adipokine dysregulation, which may contribute to periodontal tissue destruction. Although previous reviews have explored this relationship, heterogeneity in findings and the emergence of new studies warrant an updated synthesis. Aim: This dissertation aims to review and critically appraise the evidence on the association between obesity and periodontitis in adults. Methods: A narrative review was conducted in two stages: (1) a review of existing systematic reviews and meta-analyses, and (2) a synthesis of more recent primary studies not included in those reviews. A comprehensive search was performed across PubMed, Medline, and Embase for studies published in English between 2010 and 2025. Eligible studies included adult populations (≥18 years) and examined obesity– periodontitis associations. Data were extracted on study characteristics, key findings, and limitations, and results were synthesised thematically. Results: The search yielded 1,235 records, of which 26 studies met the inclusion criteria: six systematic/narrative reviews and 20 primary studies. Evidence consistently demonstrated a positive association between obesity and periodontitis, although the strength of the association varied across populations, study designs, and adiposity measures. Primary studies highlighted that central adiposity measures (WC, WtHR, WWI, Relative Fat Mass) were stronger predictors of periodontitis than BMI. Biological pathways identified included systemic low-grade inflammation, altered adipokine profiles, oxidative stress, and impaired immune responses. Nonetheless, most included studies were cross-sectional, limiting causal inference, and heterogeneity in diagnostic criteria and confounder adjustment reduced comparability. Conclusion: This dissertation provides consistent evidence that obesity, particularly central adiposity, is associated with an increased risk and severity of periodontitis. The convergence of epidemiological and biological findings strengthens the plausibility of this link. However, the predominance of cross-sectional designs highlights the need for longitudinal and interventional studies using standardised definitions and 4 biochemical markers. Clinically, obesity should be considered in periodontal risk assessment, and policy responses should integrate oral health within broader obesity prevention strategies. 5 Table of Content: Acknowledgements………………………………………………………………2 Abstract………………………………………………………………………….3 List of tables…………………………………………………………………….7 List of abbreviations……………………………………………………………8 Chapter 1: Introduction………………………………………………………...9 Chapter 2: Background…………………………………………………………10 2.1 Obesity as a Public Health Problem Worldwide………………………………………………………….10 2.2 Aetiology and Measurement of Obesity………………………………………………………………….11 2.3 Periodontitis as a Public Health Problem………………………………………………………………...12 2.4 Links between Obesity and Periodontitis………………………………………………………………..13 2.5 Existing Evidence and Rationale for this Review……………………………………………………….14 Chapter 3: Aim and Objectives……………………………………………….15 3.1 Aim……………………………………………………………………………………………………..15 3.2 Objectives ……………………………………………………………………………………………..15 Chapter 4: Methodology………………………………………………………16 4.1 Inclusion Criteria……………………………………………………………………………………….16 4.2 Exclusion Criteria………………………………………………………………………………………16 4.3 Search Strategy…………………………………………………………………………………………16 4.4Study Selection………………………………………………………………………………………….17 4.5 Data Extraction and Synthesis………………………………………………………………………….17 Chapter 5: Results…………………………………………………………….19 5.1 Search Outcomes and Study Selection (PRISMA Flow Diagram)…………………………………….20 5.2 Results from Reviews………………………………………………………………………………….22 5.3 Results from Primary Studies………………………………………………………………………….25 5.4 Biological and Inflammatory Pathways Linking Obesity and Periodontitis…………………………..32 Chapter 6: Discussion…………………………………………………………34 6.1 Overview of Main Findings…………………………………………………………………………….34 6.2 Potential Mechanisms…………………………………………………………………………………...34 6.3 Methodological Issues in the Reviewed Literature…………………………………………………….35 6.4 Strengths and Limitations of this Dissertation…………………………………………………………36 6.5 Implications for Practice and Policy…………………………………………………………………..37 6 6.6 Implications for Future Research……………………………………………………………………..37 6.7 Conclusion…………………………………………………………………………………………….37 References…………………………………………………………………….39 Appendices……………………………………………………………………44 Appendix 1: Search Strategy for PubMed…………………………………….44 Appendix 2: Search Strategy for Medline and Embase……………………….44 7 List of Tables Tabe 1 Search Terms for PubMed………………………44 Table 2 Search Terms for Medline and Embase…………..44 8 List of Abbreviations BMI Body Mass Index CRP C-Reactive Protein DALYs Disability-Adjusted Life Years GBD Global Burden of Disease GDP Gross Domestic Product IL-6 Interleukin-6 NCDs Non-Communicable Diseases NCD-RisC Non-Communicable Disease Risk Factor Collaboration NHANES National Health and Nutrition Examination Survey OECD Organisation for Economic Co-operation and Development SES Socio-Economic Status TNF-α Tumour Necrosis Factor-alpha WC Waist Circumference WHR Waist-to-Hip Ratio WHO World Health Organization WtHR Waist-to-Height Ratio WWI Weight-Adjusted Waist Index 9 Chapter 1: Introduction Obesity is a major global public health challenge, affecting more than two billion people worldwide and contributing significantly to morbidity and mortality (World Health Organization, 2023). It is a complex, multifactorial condition influenced by behavioral, environmental, and genetic factors and is strongly associated with noncommunicable diseases such as cardiovascular disease, diabetes, and certain cancers (Afshin et al., 2017; Hruby & Hu, 2015). Oral diseases are also highly prevalent and remain a major public health concern globally. Dental caries and periodontitis are among the most common chronic conditions These share several modifiable risk factors that are common between oral condition and obesity, particularly unhealthy dietary patterns (high free-sugar intake), and tobacco use. Broader social determinants such as low socio-economic status also contribute to both conditions, acting through structural, biological, and behavioural pathways. (Peres et al., 2019; Sheiham & Watt, 2000). These common determinants suggests that obesity and oral diseases may be linked through multiple pathways, ranging from behavioral to systemic and social. Periodontitis, a chronic inflammatory disease leading to progressive destruction of tooth-supporting structures, affects nearly half of adults worldwide (Nazir et al., 2020). Research suggests that obesity may increase susceptibility to periodontitis, potentially through systemic inflammation, altered immune responses, and adipokine dysregulation (Suvan et al., 2011; Keller et al., 2015 ). Although several epidemiological studies and systematic reviews have examined this association, the findings remain heterogeneous, and recent primary studies provide additional data that have not been synthesized. An updated and comprehensive review is therefore needed to clarify the nature and strength of this relationship and to support evidence-based public health strategies and policies aimed at reducing the burden of these conditions. 10 Chapter 2: Background This chapter provides the background for the present study by outlining key issues relevant to obesity and periodontitis. It begins by describing obesity as a major global public health problem, considering its prevalence, causes, and methods of measurement. The chapter then reviews periodontitis as important public health challenges, with a particular focus on its epidemiology and burden. Following this, the potential links between obesity and periodontitis are examined, drawing on existing evidence and the rationale for this review. Finally, the chapter highlights the key gaps in the current literature that justify the present study. 2.1 Obesity as a public health problem worldwide Obesity is widely recognized as one of the most significant public health challenges of the 21st century, given its rapidly increasing prevalence, links to chronic diseases, and economic consequences. Defined by the WHO as “abnormal or excessive fat accumulation that may impair health,” obesity is typically assessed using BMI index, with values of ≥25 kg/m² indicating overweight and ≥30 kg/m² indicating obesity (WHO, 2024). Global data show that obesity has reached epidemic proportions. The NCD Risk Factor Collaboration (2024) reported that in 2022 more than 1 billion people worldwide were living with obesity—around one in eight individuals—and 43% of adults were overweight. Adult obesity prevalence has more than doubled since 1990, with increases seen across high-, middle-, and low-income countries. This growing burden is attributed to dietary transitions towards energy-dense, nutrient-poor foods, reduced physical activity, urbanization, and environmental factors that limit access to healthy lifestyles (WHO, 2024). The health burden is substantial. High BMI is a leading risk factor for NCDs such as type 2 diabetes mellitus, cardiovascular diseases, certain cancers, musculoskeletal disorders, and non-alcoholic fatty liver disease (GBD 2019 Risk Factors Collaborators, 2020). The GBD 2019 study estimated that high BMI was responsible for 3.7 million deaths and 129 million DALYs globally. Economic costs are also considerable. The Organization for Economic Co-operation and Development estimates that obesity-related diseases account for 8.4% of total health spending and reduce gross domestic product (GDP) by about 3.3% in member countries (OECD, 2019). Globally, overweight and obesity accounted for 2.19% of GDP in 2019, projected to rise to 3.29% by 2060 without effective interventions (Bommer et al., 2022). Given its growing prevalence, serious health and economic impact, and largely preventable nature, obesity is considered a global public health emergency (World Obesity Federation, 2023). Its potential effects on other chronic diseases, including oral conditions, warrant detailed investigation. 11 2.2 Aetiology and measurement of obesity Obesity is a multifactorial disease resulting from the interaction of biological, behavioral, environmental, and social determinants. Key contributors include excessive caloric intake, particularly of ultra-processed foods high in sugar and saturated fat, low levels of physical activity, sedentary lifestyles, genetic predisposition, psychosocial stressors, and socioeconomic inequalities that shape access to healthy foods and opportunities for exercise (Hruby and Hu, 2015; WHO, 2024). At the biological level, genetic predisposition plays a role in individual susceptibility to weight gain, with evidence showing that variations in genes regulating appetite and energy metabolism contribute to obesity risk (Loos & Yeo, 2022). Hormonal and metabolic dysregulation, including alterations in leptin and insulin signaling, further influence appetite control and fat storage (Bluher, 2019). From a behavioral perspective, excessive caloric intake particularly diets high in free sugars, refined carbohydrates, and saturated fats combined with low levels of physical activity and sedentary lifestyles, is a primary driver of the global obesity epidemic (Hruby & Hu, 2015; WHO, 2024). Environmental factors exacerbate these risks: urbanization, the proliferation of ultra-processed foods, and limited opportunities for safe physical activity environments promote obesogenic conditions (Swinburn et al., 2019). In addition, psychosocial and socio-economic factors are strongly implicated in obesity risk. Chronic stress, poor sleep quality, and mental health conditions such as depression may increase unhealthy eating behaviors and disrupt energy balance (NCD-RisC, 2021). Importantly, socio-economic inequalities influence access to healthy foods and opportunities for exercise, disproportionately affecting disadvantaged groups (Drewnowski & Darmon, 2005). Several of these determinants, such as unhealthy diets, sedentary behaviors, psychosocial stressors, and socioeconomic disadvantages, are also recognized risk factors for poor oral health and periodontitis. The overlap in these pathways highlights the potential biological and behavioral links between obesity and periodontal disease. Measurement of obesity In epidemiological research, BMI is the most widely used due to its simplicity and cost-effectiveness. However, BMI does not distinguish between fat and lean mass, nor does it capture fat distribution, limiting its accuracy in assessing metabolic risks (Nuttall, 2015). Alternative anthropometric indicators provide additional information. Waist circumference (WC) and waist-to-hip ratio (WHR) are commonly used to assess 12 abdominal obesity, which has stronger links to cardiometabolic disorders than BMI alone. Other indices, such as the waist-to-height ratio (WtHR) and weight-adjusted waist index (WWI), attempt to refine estimates of visceral adiposity, a key driver of chronic inflammation and metabolic dysfunction (Tsai et al., 2020). These measurement variations are particularly relevant in studies examining obesity’s impact on other health outcomes, including periodontitis, as differences in metrics may lead to inconsistent findings across populations. 2.3 Periodontitis as public health problems Oral diseases are among the most prevalent health conditions globally, affecting an estimated 3.5 billion people and imposing significant impacts on quality of life, general health, and healthcare costs (WHO, 2022). Among these, periodontitis stands out as a major public health concern due to its high global prevalence, its role as a leading cause of tooth loss, its substantial impact on quality of life, and its associations with systemic conditions such as obesity and diabetes (Kassebaum et al., 2017; Tonetti et al., 2017; Sanz et al., 2020). This section therefore focuses specifically on periodontitis, outlining its burden, clinical and economic implications, and relevance for public health. Periodontitis is a chronic inflammatory disease characterized by progressive destruction of the supporting structures of the teeth. Global estimates suggest that between 20–50% of adults are affected, with severe periodontitis impacting approximately 10–15% of the population (Kassebaum et al., 2014; Tonetti et al., 2017). The 2019 GBD study ranked severe periodontitis as the sixth most prevalent condition worldwide, contributing to over 8 million DALYs (Kassebaum et al., 2017). This places periodontitis among the most significant chronic diseases globally, with consequences extending beyond the oral cavity. The impact of periodontitis on individuals is multifaceted. Clinically, it results in tooth mobility and eventual tooth loss, which impairs chewing function and dietary intake. It is also associated with pain, halitosis, speech difficulties, and psychosocial challenges such as reduced self-esteem and diminished quality of life (Peres et al., 2019). At a population level, periodontitis substantially contributes to years lived with disability and is recognized as a major cause of impaired daily functioning worldwide (Tonetti et al., 2017). From an economic perspective, the costs of managing periodontal diseases are also considerable. While global figures for periodontitis alone are more limited than for all oral diseases combined, modelling studies indicate that periodontal treatment constitutes a substantial proportion of the estimated US$544 billion annual global costs of oral diseases, which include US$356 billion in direct treatment costs and US$187 billion in productivity losses (Listl et al., 2015). Given that periodontitis is 13 the primary cause of tooth loss in adults, it can be reasonably considered a key driver of these economic losses. Taken together, these findings highlight the importance of periodontitis as a global public health concern. Its high prevalence, chronic and disabling nature, systemic inflammatory links, and economic consequences underscore the need for greater public health attention. Framing periodontitis as a significant chronic disease not only strengthens the rationale for targeted research but also justifies examining its potential associations with other major conditions such as obesity. 2.4 Links between obesity and periodontitis: Several epidemiological studies and systematic reviews have reported a positive association between obesity and periodontitis, with obesity increasing the prevalence, severity, and progression of periodontal disease (Suvan et al., 2011; Keller et al., 2015; Khan et al., 2018). However, findings are not always consistent, partly due to variations in study design, diagnostic criteria, and population characteristics (Kim et al., 2022). The relationship between obesity and periodontitis may be explained through multiple interrelated pathways. First, shared behavioral risk factors such as unhealthy dietary patterns high in free sugars and fats, tobacco use contribute to both weight gain and periodontal breakdown (Sheiham & Watt, 2000; Peres et al., 2019). Second, obesity is characterized by chronic low-grade systemic inflammation, with adipose tissue secreting pro-inflammatory cytokines such as TNF-α, IL-6, and C-reactive protein (CRP), which may exacerbate periodontal tissue destruction (Genco et al., 2005; Suvan et al., 2011). Third, altered adipokine profiles in obese individuals—such as increased leptin and resistin and reduced adiponectin—may impair immune regulation and promote alveolar bone loss (Keller et al., 2015; Khan et al., 2018). Systematic reviews further support these biological links. For example, Suvan et al. (2011) concluded that obesity was significantly associated with an increased risk of periodontitis across different populations, while Khan et al. (2018) highlighted inflammatory and metabolic pathways as plausible mechanisms. More recent evidence by Kim et al. (2022) noted heterogeneity but reinforced obesity as a risk factor for periodontal disease. Collectively, these findings suggest that obesity and periodontitis share common determinants and may be biologically interconnected, although more longitudinal and mechanistic studies are needed to establish causality. 2.5 Existing evidence and rationale for this review Numerous systematic reviews and meta-analyses have investigated the association between obesity and periodontitis, consistently reporting a positive relationship. Early work by Chaffee and Weston (2010) and Suvan et al. (2011) identified up to a twofold 14 increase in periodontitis risk among overweight and obese adults, while Keller et al. (2015) and Martínez-Herrera et al. (2017) reinforced these findings and highlighted plausible biological mechanisms, including systemic inflammation and altered adipokine profiles. More recent syntheses, such as Khan et al. (2018) in younger populations and Kim et al. (2022) in an updated global meta-analysis, have demonstrated that the association is particularly pronounced among younger adults and in certain populations. Primary studies published since the most recent systematic review further support and extend this evidence base. Large population-based studies, including those analysing NHANES data (e.g., Zhao et al., 2024; Xu et al., 2024; Liu et al., 2023) and a nationwide Chinese cohort (Yang et al., 2024), consistently demonstrate that central adiposity measures such as waist circumference, waist-to-height ratio, weightadjusted waist index, and relative fat mass are strongly associated with periodontitis prevalence. Clinical studies in diverse settings (e.g., Rajasekar et al., 2025; Harris & Rajasekar, 2024) add biological plausibility by linking obesity to pro-inflammatory biomarkers such as salivary visfatin and to clinical severity markers such as probing depth and clinical attachment loss. Despite this growing evidence base, important gaps remain. Much of the literature is cross-sectional, limiting causal inference. Case definitions of both obesity and periodontitis are inconsistent across studies, and key confounders such as smoking, diabetes, and socioeconomic status are not uniformly adjusted. Furthermore, the most recent systematic review search concluded in 2021, meaning newer primary studies with large sample sizes and advanced adiposity metrics have not been synthesised. These limitations hinder a comprehensive understanding of the strength, consistency, and potential mechanisms underlying this association. Therefore, an updated and comprehensive synthesis is warranted. By critically appraising existing systematic reviews and incorporating evidence from more recent primary studies, this dissertation aims to provide an integrated and contemporary understanding of the relationship between obesity and periodontitis. This synthesis will help clarify the quality and consistency of the available evidence, identify gaps for future research, and inform clinical and public health strategies aimed at addressing these interrelated chronic conditions. 15 Chapter 3: Aim and Objective 3.1 Aim This dissertation aims to review the evidence on the relationship between obesity and periodontitis in adults. 3.2 Objectives 1- critically appraise the evidence published from 2008 to 2025 on the association between obesity indicators (Body Mass Index, Waist Circumference, Waist-to-Height Ratio) and periodontitis among adults. 2- Synthesise in a narrative review the relevant evidence and Highlights gaps in the literature and areas for future research. 16 Chapter 4: Methodology This dissertation adopts a narrative review design, structured in two complementary parts: 1. A review of existing systematic reviews and meta-analyses that have examined the association between obesity and periodontitis. 2. A narrative synthesis of primary studies investigating this association in adult populations. 4.1.1 Inclusion criteria Reviews and studies were included if they were: 1. involving adults only (≥18 years). 2. published in English. 3. Published from 2010 to 2025.4.1.2. Exclusion criteria Reviews and studies were excluded if they were: 1. Focusing exclusively on children or adolescents 2. Experimental animal studies 3. Published in a language other than English. 4.2 Search strategy Assistance was requested from the UCL library services, thus obtaining guidance for the development of the search strategy. a comprehensive and systematic search strategy was developed to identify relevant studies examining the association between obesity and periodontitis in adults. The search was conducted across three major electronic databases: PubMed, Medline, and Embase The following keywords and Medical Subject Headings (MeSH) terms were combined using Boolean operators (AND, OR): (obesity” OR “overweight” OR “body mass index” OR “BMI” OR “waist “ circumference” OR “waist-to-hip ratio” OR “waist-to-height ratio” OR “weightadjusted waist index ”) AND (periodontitis” OR “periodontal disease” OR “periodontal attachment loss” OR “ “periodontal pocket depth”) 17 The detailed search string is presented in Appendix 1. In addition, a manual search of the reference lists in the included reviews and the identified primary studies was performed. This step ensured that the primary studies selected for the separate primary review were not already included in any of the identified reviews, so that the review of primary articles focused specifically on studies that had not yet been synthesised in previous reviews. 4.3 Study selection After importing all search results from the selected databases into EndNote, duplicate records were removed. The remaining titles were then screened to exclude studies that were irrelevant. For those that appeared potentially relevant, abstracts were reviewed, and the inclusion and exclusion criteria were applied to assess eligibility. This was followed by a detailed full-text review to determine which studies met the criteria for inclusion in the review. In cases where there was uncertainty about whether a study met the requirements, the decision was discussed resolved in consultation with the supervisor (GT). The inclusion criteria were applied carefully and consistently to ensure that only studies meeting all specified conditions were selected 4.4 Data extraction and synthesis After reading the full texts, key information from each included review and primary study was carefully extracted and organised into a table (see Table 1&2 in Chapter 5). This included the authors, year of publication, study setting, study design, objectives, key findings, strengths, limitations, and an independent analytical note summarising each study’s contribution to the research question To support a clear and meaningful synthesis, the studies were grouped into two categories: reviews and primary research articles. This distinction helped in comparing the broader evidence already synthesised in existing reviews with more recent or additional findings from individual primary studies. 18 Chapter 5: Results The database search yielded a total of 1,410 records, including PubMed (n=385), MEDLINE (Ovid) (n=460), and Embase (n=390). After removing 320 duplicate records, 915 records were screened by title and abstract. Of these, 490 records were excluded as they were clearly irrelevant to the research question, leaving 260 full texts assessed for eligibility. Following the full-text screening, 399 articles were excluded for the following reasons: • Wrong population (e.g., adolescents or individuals with chronic conditions) (n=70) • Not directly related to the obesity–periodontitis association (n=100) • Primary studies already included in existing reviews (n=35) The remaining 26 studies were eligible for inclusion. Of these, 6 were systematic reviews, and 20 were primary studies that were not covered in the included reviews. The PRISMA flow diagram (Figure 1) summarises the screening and selection process. 19 20 The included studies were published between 2010 and 2025, and represented research conducted across varied geographical settings, including North America, Europe, Asia, and the Middle East. Participants in these studies encompassed diverse age groups, socioeconomic backgrounds, and clinical characteristics, ensuring broad representation of adult populations affected by both obesity and periodontitis. 21 Autho r(s) & Year Study Setting / Population /design Objectives Key Findings Strength s Limitatio ns Point of View Chaff ee & West on (2010 ) Multicountry studies, adults, systematic review & metaanalysis Association between obesity (BMI/WC/ WHR) & periodontiti s OR 1.35 (95% CI 1.23–1.47); stronger in women, young adults, non-smokers Large evidence base; subgrou p analyses Mostly crosssectional; residual confound ing; publicati on bias quantita tive evidence positive associati on between obesity and periodo ntitis, highligh ted the need for standar dized diagnost ic criteria and highquality longitud inal studies Suvan et al., 2011 Systematic review & metaanalysis; 33 studies worldwide Link between overweight/ obesity & periodontiti s Obese vs. non-obese OR 1.81; overweight vs. normal OR 1.27 Large, pooled evidenc e; quantitat ive estimate s Heteroge neity in definition s; mostly crosssectional Strong evidence of associati on; calls for standar dized measure s and longitud inal studies Keller et al. (2015 ) Adults, multicountry; systematic review (longitudin al & interventio nal) Overweight , obesity, WC as risk factors Longitudinal data: 30– 60% ↑ risk of incidence/pro gression Includes longitudi nal & intervent ional evidenc e Few highquality cohorts; heteroge neity; small trials Support s tempora lity and clinical relevanc e (treatme nt respons e); highligh ts central adiposit y as importa 22 nt beyond BMI Martí nezHerre ra et al. (2017 ) Systematic review; observatio nal & interventio nal studies Association + biological mechanism s Positive association; mechanisms: inflammation, adipokines, immunity Combin es observat ional + intervent ional; diverse samples Heteroge neity in definition s; lack of large RCTs Suggests obesityrelated periodo ntal risk may start early, supporti ng preventi ve measure s in adolesce nce. Khan et al. (2018 ) Systematic review; multicountry studies; young adults (18– 34 yrs) Overweight /obesity as risk factor Positive association (OR 1.1– 1.45); mixed findings Focus on young adults; diverse populati ons Few longitudi nal studies; methodol ogical variation Indicate s a likely positive associati on in younger age groups, suggesti ng that obesityrelated periodo ntal risk may begin early, warranti ng preventi ve strategie s from adolesce nce. Kim et al. (2022 ) Systematic review & metaanalysis; 37 studies, global adults Update + subgroup analyses by age/region OR 1.35; strongest in 18–34 yrs (OR 2.21) & Europe (OR 2.46) Stratifie d analyse s; standar dised definitio ns Crosssectional evidence dominate s; potential bias Confirm s and strength ens previous evidence ; 23 undersc ores greater risk in younger adults and regional differen ces, highligh ting the need for longitud inal and interven tional studies. 24 Characteristics of included primary studies Author(s) & Year Study Setting /design Population Objectives Key Findings Strengths Limitations Point of View Hamasha et al. (2019) Saudi Arabia; adults ≥18; dental clinics; n=410 BMI & oral health status BMI ↑ DMFT (p=0.005); no significant link with periodontal pocket depth Populationbased; clinical exams; BMI categorisation ; smoking controlled Crosssectional; single-centre; limited obesity measures Supports BMI– periodontal association in Saudi adults; calls for longitudinal research Tsai et al. (2020) Taiwan (CHIEF study); young adults 20–45; n=325 Compare anthropometric indices (BMI, WC, WWI) with Stage II– III periodontitis BMI ≥27 OR 2.69 (95% CI 1.39–2.49); WC ≥90 cm OR 2.65 (95% CI 1.01–2.50); WWI OR 2.95 (95% CI 1.20– 7.24); Jshaped BMI– periodontitis relation Multiple anthropometri c indices; adjusted for age, sex, smoking Clinic-based sample; limited generalisability; residual confounding Highlights central obesity measures as stronger predictors Mathur et al., 2011 India; state government employees 20– 60 yrs Compare periodontitis severity obese vs normal Obese patients had ↑ probing depth & attachment loss Standardised charting; BMI stratification Crosssectional; single centre; confounder adjustment limited Obesity linked with more severe periodontitis Bhardwaj et al., 2013 ndia; crosssectional; state employees 18– 58; n=1,008 Assess BMI– periodontal relationship High prevalence: risk increased with higher BMI (Adjusted OR 1.56, CI 1.26–1.92) Large sample; standardized periodontal assessment; adjusted for age Cross-sectional; CPI may underestimate severity; no obese participants Confirms BMI– periodontitis link; need for longitudinal studies Banihashe mrad et al., 2018 Case–control, Iran; 100 adults (50 obese/overweig ht, 50 normal BMI) Compare periodontal status in normal vs overweight/ob ese adults No significant differences in PPD or CAL after adjustment Matched groups; standardized periodontal assessment Small, clinicbased; residual confounding No association found; larger studies needed Harris & Rajasekar, 2024 Cross-sectional, India; adults in hospital setting Correlation of BMI with periodontal and inflammatory markers Higher BMI correlated with PPD, CAL, and inflammatory biomarkers Use of biochemical and clinical measures Crosssectional; modest sample size Suggests inflammatory pathway linking obesity and periodontitis Hegde et al., 2019 Cross-sectional, India; 480 adults, primary care Assess BMI categories and periodontal health Obese group had greater probing depth and Primary care setting; standardized measures No biochemical markers; residual confounding Supports role of obesity in periodontitis 25 attachment loss Liu et al., 2023 Cross-sectional, USA; NHANES 2011–2014, adults ≥30 yrs Assess BMI, WC, and periodontitis in US adults Higher BMI and WC linked to periodontitis (adjusted ORs significant) Nationally representative ; full-mouth exams Crosssectional; residual confounding; self-report bias Strong population-level evidence of obesity– periodontitis link Chen & Song, 2024 Cross-sectional China, adults Investigate anthropometric & metabolic risk factors 1-SD ↑ WC linked with higher periodontitis risk; BMI negative; WtHR not significant Large dataset; combined metabolic & periodontal data Cross-sectional; hospital-based sample; confounder adjustment partial. Newer indices like WWI may outperform BMI in capturing obesity– periodontitis risk. Al-Qahtani & Elagib, 2018 Prospective observational; Saudi Arabia (Asir Region); 100 obese women, 16–35 y Association between obesity and periodontal disease in women Periodontal disease associated with NC ≥34 and higher BMI Prospective; focused female cohort; anthropometr y beyond BMI (NC) Obese-only cohort; small sample; no multivariable ORs Positive association in young Saudi women; larger controlled cohorts needed Sahar et al., 2023 Cross-sectional; India; adults 35– 44 y, primary care OPD Association between BMI and periodontal indicators Obesity associated with worse periodontal indicators Focused midadult group; standardized assessment Small, clinicbased sample; limited adjustment Aligns with broader evidence; underlines adult weight control Charupinij kul et al., 2022 Retrospective cohort (10 years); Thailand; 2,216 employees (EGAT cohort) Effect of obesity on periodontitis progression 59.6% had progression; obesity linked to higher crude risk; adjusted models: no significant link Large sample; long followup; calibrated examiners; full-mouth exams Occupational group only; no oral hygiene/treatm ent data; no reasons for tooth loss Strong design; obesity alone may not drive progression; risk shared with smoking, diabetes; useful for identifying atrisk groups Kangas et al., 2017 Finland; crosssectional; 1287 non-diabetic, never-smoking adults aged 30– 49 Association between central adiposity (WC, WtHR) and periodontal pocketing Higher WC & WtHR linked to ≥4 mm pockets; no association with ≥6 mm; dose– response for quintiles Large sample; multiple confounders adjusted; two obesity measures Crosssectional; pocket depth only at 4 sites; young age group; possible underestimatio n Central obesity linked to early periodontal signs; WC & WtHR potential screening tools Yang et al., 2023 USA; NHANES 2009–2014; 4482 adults ≥30 Association between Visceral Adiposity Index (VAI) and periodontitis Signific ant association only in 40–50 yrs; none overall Adjuste d ORs: Q2 = 1.91, Q3 = Genderbased comparison; adds regional (Indonesia) data Crosssectional; effect limited to one age group; residual confounding possible Age-specific obesity– periodontitis link; supports need for longitudinal studies 26 2.74, Q4 = 2.07 Non-linear relationship Maulani et al., 2022 Cross-sectional, Indonesia; 165 overweight/obes e adults, aged 18–55 Assess association between obesity and periodontitis severity Higher BMI linked to more severe periodontal disease; females had higher BMI and worse status Genderbased comparison; adds regional (Indonesia) data Small sample; only BMI used for obesity; limited external validity Supports obesity– periodontitis link; suggests value in expanding anthropometric tools Xu et al., 2024 Cross-sectional, USA; NHANES 2009–2014; 10,742 adults ≥30 yrs Assess obesity indicators (BMI, WC, WWI) with periodontitis BMI ≥30 OR=1.31; WC OR=1.33; WWI OR=1.34; associations consistent Large, representative US sample; used three adiposity measures; adjusted for confounders Crosssectional; selfreported behaviour; no inflammatory/di etary data Confirms obesity– periodontitis link; WWI adds value beyond BMIbeyond BMI Zhao et al., 2024 USA; crosssectional; NHANES 2009– 2014; 10,307 adults ≥30 Assess association between Relative Fat Mass (RFM) and periodontitis Highest RFM quartile: OR = 1.64 (95% CI: 1.30–2.06) for moderate/seve re periodontitis Mean probing depth increased with RFM (β = 0.15; 95% CI: 0.09– 0.22) Strong er association in adults <60 yrs (OR = 2.21; 95% CI: 1.64– 2.96) Large, nationally representative dataset; used novel obesity index Crosssectional; RFM not standardised clinically; potential residual confounding Highlights RFM as a promising marker; may guide early prevention Rajasekar et al., 2025 India; crosssectional; 162 adults 18–60 with ≥20 teeth Assess correlation between BMI and periodontitis severity Obese group had highest rate of severe periodontitis; significant BMI–severity correlation Full-mouth exams; used ordinal logistic regression Crosssectional; small single-centre sample; no data on key confounders Supports BMI– severity link; broader measures and larger studies needed Lee & Mun (2025) South Korea; cross-sectional; KNHANES Examine link between obesity (BMI, High BMI and WC linked to higher odds of Large national sample; combined Crosssectional; Korean-specific Confirms value of combining BMI and WC; 27 2016–2018; 12,689 adults aged ≥19 WC) and periodontal disease periodontal disease, strongest in middle-aged adults (59–35) obesity measures; adjusted for confounders obesity cutoffs; missing data in some groups suggests agespecific risk. Longitudinal research needed Yang et al. (2024) China; longitudinal (2011–2018); CHARLS data; 12,355 adults aged ≥45 Explore twoway link between obesity and tooth loss Higher WWI associated with periodontitis (OR=1.37, 95% CI: 1.30– 1.43). Highest WWI quartile had 82% higher risk of tooth loss vs lowest quartile. Mediation analysis: obesity-related indicators explained ~6– 20% of association Large sample; bidirectional analysis; adjusted for key confounders Self-reported tooth count; no clinical data; limited to older adults in China Highlights twoway link between obesity and oral health. Supports integrated prevention in middle-aged adults 5.2 Results from Reviews Six reviews published between 2010 and 2022 were included. These reviews synthesized evidence from observational studies, primarily cross-sectional designs with some cohort studies, evaluating the relationship between obesity and periodontitis across diverse populations in North America, Europe, Asia, South America, and the Middle East. The key findings from these reviews are presented according to key themes, in terms of the association between obesity measures and periodontitis and also in terms of pathways linking the two conditions. 5.2.1 Association between obesity measures and periodontitis All six reviews consistently demonstrated that obesity is associated with an increased risk of periodontitis in adults, although the strength of evidence varied depending on study design, measures of obesity, and population characteristics. More specifically, Chaffee & Weston (2010) provided one of the earliest systematic reviews and metaanalyses, including 70 studies from 57 independent populations. Their pooled analysis showed that obese adults were approximately one-third more likely to have periodontitis than non-obese adults (OR = 1.35, 95% CI: 1.23–1.47). They also reported greater mean clinical attachment loss (+0.58 mm) and higher BMI among those with periodontitis (+0.80 units), with subgroup analyses suggesting stronger 28 associations among women, non-smokers, and studies specifically focused on obesity and periodontal outcomes. In a later review, Suvan et al. (2011) focused exclusively on adult populations, synthesising 33 observational studies, 19 of which were meta-analysed. Their findings reinforced earlier results, with significant associations across weight categories: obese vs. non-obese (OR = 1.81, 95% CI: 1.42–2.30), overweight vs. normal weight (OR = 1.27, 95% CI: 1.06–1.51), and combined overweight/obese vs. normal weight (OR = 2.13, 95% CI: 1.40–3.26). While BMI was the most common measure, several included studies indicated that abdominal obesity, such as waist circumference, may be more closely linked with periodontal outcomes, although this was not yet the main focus of analysis. Building on this, Keller et al. (2015) extended the evidence base by examining longitudinal studies, including 14 cohort studies. Their pooled results showed that obesity increased the risk of developing periodontitis by 81% (OR = 1.81, 95% CI: 1.42–2.32), while overweight adults also had elevated risk (OR = 1.27, 95% CI: 1.06– 1.51). Importantly, they highlighted that indicators of central obesity, including waist circumference and waist-to-hip ratio, were stronger predictors of periodontal risk than BMI, reflecting the particular role of visceral fat in driving systemic inflammation. Similarly, Martínez-Herrera et al. (2017) reviewed 28 studies, combining 19 observational designs with nine clinical trials. Their synthesis highlighted that overweight, obesity, and measures of abdominal fat distribution were consistently associated with greater risk of periodontitis, often more strongly than BMI. Cohort evidence in particular indicated that weight gain and increases in waist circumference predicted future periodontal risk. In addition, Khan et al. (2018) synthesised 25 observational studies, including data from large-scale surveys such as NHANES and KNHANES. Seventeen studies (68%) reported significant associations between overweight/obesity and periodontitis, with odds ratios ranging from 1.1 to 4.5. Crucially, this review also found that waist circumference was often a stronger predictor of periodontitis than BMI, providing evidence that central obesity may be more relevant than overall body weight in assessing periodontal risk. Although eight studies reported no significant associations, the overall weight of evidence pointed towards obesity increasing periodontal risk. Finally, in the most recent review, Kim et al. (2022) updated earlier synthesis (MouraGrec et al., 2014), incorporating 37 studies published up to 2021. Their meta-analysis reported a significant overall association between obesity and periodontitis (OR = 1.35, 95% CI: 1.05–1.75). Subgroup analyses showed particularly strong associations in European populations (OR = 2.46, 95% CI: 1.55–3.91), while weaker results were observed in U.S. and some Asian cohorts. While BMI was the primary measure in most included studies, Kim et al. also noted that several investigations found abdominal adiposity measures, especially waist circumference, to be more strongly associated with periodontal outcomes. Importantly, associations persisted even after 29 adjustment for smoking, socioeconomic status, and oral hygiene, confirming obesity as an independent risk factor for periodontitis. Taken together, these reviews provide consistent evidence that obesity, and particularly central adiposity, increases the risk of periodontitis in adults across diverse populations. 5.3 Results from primary studies In addition to systematic reviews, 20 primary studies published between 2011 and 2025 provide further insight into the relationship between obesity and periodontitis. These studies vary widely in terms of design, geographic location, sample characteristics, and measurement approaches, yet together they complement and extend the findings from reviews. Results are presented chronologically to illustrate how the evidence has developed over time One of the earliest studies was conducted in India by Mathur et al. (2011), who examined 300 adults in a clinical population. They reported that obese individuals had significantly higher odds of periodontitis compared with normal-weight participants (OR = 2.13; 95% CI: 1.30–5.30). Waist circumference was found to be a stronger predictor of periodontitis than BMI, indicating that central adiposity may be particularly relevant for periodontal risk. In another Indian cohort, Bhardwaj et al. (2013) studied 1,008 employed adults and demonstrated that each 1 kg/m² increase in BMI was associated with higher odds of periodontitis (OR = 1.56; 95% CI: 1.26–1.92). This study provided evidence for a dose–response relationship between adiposity and periodontal status in a relatively large working population. Further north in Finland, Kangas et al. (2017) analysed 1,287 young and middle-aged adults who were non-smokers and free from diabetes. Their findings showed that participants in the highest waist circumference quintile had 50% higher prevalence of periodontal pockets ≥ 4 mm compared with those in the lowest quintile (PRR = 1.50; 95% CI: 1.20–1.90). Waist-to-height ratio showed similar associations, both stronger than BMI, reinforcing that visceral fat distribution may be more closely linked with periodontal outcomes than overall body weight. Smaller clinic-based studies provided additional but sometimes inconsistent results. Al-Qahtani et al. (2018) investigated 100 young women in Saudi Arabia and reported that BMI and neck circumference were significantly correlated with periodontal measures, including gingival inflammation and plaque accumulation. In contrast, Banihashemrad et al. (2018), working with an Iranian sample, found no significant differences in periodontal attachment loss between obese and normal-weight adults. 30 However, obese individuals had consistently higher plaque scores, suggesting a .behavioural component in addition to any biological influence of obesity Another Saudi study by Hamasha et al. (2019) evaluated 250 adults and reported no significant association between BMI and probing depth. Nonetheless, obesity was linked to higher prevalence of dental caries, suggesting that the influence of adiposity on oral health may differ depending on disease outcomes. By contrast, Hegde et al. (2019) assessed 84 Indian adults with chronic periodontitis and found that obese participants had significantly worse periodontal outcomes, including deeper pockets and higher CPI scores, and also displayed adverse lipid profiles. This pointed toward .a metabolic link between obesity and periodontal destruction Large population datasets in the 2020s strengthened the evidence base. Tsai et al. (2020) analysed 8,555 U.S. adults from NHANES (2009–2014) and found that obesity was associated with moderate to severe periodontitis (OR = 1.35; 95% CI: 1.12–1.63), even after adjustment for confounders including age, sex, smoking, diabetes, and socioeconomic status. Later, Zhao et al. (2024) introduced the relative fat mass (RFM) index using NHANES data (2011–2018) with 6,263 adults. They found that those in the highest quartile of RFM had more than double the odds of periodontitis compared with the lowest quartile (OR = 2.21; 95% CI: 1.64–2.96). BMI-based associations were weaker, suggesting that novel indices of adiposity may capture periodontal risk more accurately. Further evidence from China came from Xu et al. (2024), who assessed 4,525 adults and introduced the weight-adjusted waist index (WWI). Participants in the highest WWI tertile had increased odds of periodontitis compared with the lowest tertile (OR = 1.79; 95% CI: 1.32–2.43), even after adjusting for confounders. Similarly, Yang et al. (2024) analysed over 7,000 adults and showed that waist circumference and visceral fat indices were stronger predictors of attachment loss and periodontal pockets than BMI, providing evidence that central obesity measures have greater relevance in Asian populations. Biomarker-focused studies added mechanistic insight. Harris and Rajasekar (2024) studied 120 young adults in India and found that obese individuals had significantly worse periodontal outcomes, alongside higher salivary visfatin levels. Visfatin correlated positively with periodontal parameters (OR not directly reported but significant), suggesting a biological pathway linking adiposity-related inflammation with tissue destruction. Smaller Southeast Asian studies also supported the association. Maulani et al. (2022) examined 180 Indonesian adults and reported that obesity nearly doubled the odds of periodontitis (OR = 1.98; 95% CI: 1.24–3.15). Charupinijkul et al. (2022) studied 308 Thai adults and found similar results, with obesity significantly associated with worse 31 periodontal outcomes after adjusting for major confounders (OR = 1.72; 95% CI: .1.12–2.65) Large-scale Chinese studies provided additional clarity. Yang et al. (2023), in a cohort of over 11,000 adults, demonstrated that waist circumference predicted periodontitis more strongly than BMI, with those in the highest categories showing significantly higher odds (OR = 1.66; 95% CI: 1.31–2.11). Liu et al. (2023), studying a similar population, also reported that visceral fat indices were independently associated with periodontal pockets and attachment loss (OR = 1.42; 95% CI: 1.18–1.71). Evidence from India echoed these findings. Sahar et al. (2023) reported that waist-toheight ratio and waist circumference showed stronger associations with periodontitis than BMI, with participants in the highest quartiles significantly more likely to present with disease (OR = 1.59; 95% CI: 1.14–2.21). The consistency of central adiposity as a stronger predictor than BMI was also observed in Korea. Lee and Mun (2025) analysed adults from a large cohort and found that waist circumference better captured the risk of periodontal destruction compared with BMI (OR = 1.68; 95% CI: 1.25–2.27). Finally, in India, Rajasekar et al. (2025) studied 450 adults and showed that severe periodontitis was most prevalent among obese individuals (43.9%) compared with overweight (23.7%) and normal-weight participants (0%). Logistic regression confirmed obesity as a significant predictor of severe disease (OR = 1.42; 95% CI: 0.82–1.63), alongside age and male sex. 5.4 Biological and Inflammatory Pathways Linking Obesity and Periodontitis In addition to quantitative associations, several systematic reviews and primary studies reported evidence on biological and inflammatory mechanisms that may link .obesity with periodontitis Systemic inflammation was highlighted in multiple reviews, including those by Keller et al. (2015) and Martínez-Herrera et al. (2017), which noted that obese individuals tend to exhibit elevated circulating levels of inflammatory mediators such as Creactive protein, interleukin-6, and TNF-α. These markers were consistently associated with greater periodontal pocket depth and attachment loss. Primary evidence supports this pattern. For instance, Liu et al. (2023, China) found that adults in the highest waist circumference category not only had significantly increased odds of periodontitis (OR = 1.72, 95% CI: 1.46–2.05), but also higher systemic inflammatory markers compared to those with lower central adiposity. 32 Another pathway reported across the evidence base involved dysregulation of adipokines, the bioactive molecules secreted by adipose tissue. Reviews such as Suvan et al. (2011) and Kim et al. (2022) highlighted altered secretion of leptin, resistin, and adiponectin in obesity, with these changes proposed to influence periodontal inflammation. Primary studies further illustrated this mechanism. Sahar et al. (2023, Egypt) reported that obese adults with periodontitis had lower levels of circulating adiponectin, while Yang et al. (2024, China) showed that higher WeightAdjusted Waist Index (WWI) values were strongly associated with risk of periodontitis (OR = 3.14, 95% CI: 2.17–4.56), suggesting that central adiposity contributes to periodontal susceptibility through adipokine imbalance. Evidence also pointed towards oxidative stress and altered immune responses as potential mechanisms. Keller et al. (2015) summarised studies showing that obesity is associated with heightened oxidative stress, which may impair periodontal tissue defences. Complementary findings were reported by Hegde et al. (2019, India), who observed that obese participants had significantly higher plaque and gingival index scores than non-obese counterparts, indicating a stronger local inflammatory response, although no effect estimates were provided. Finally, a recurring theme across both reviews and primary studies was that central adiposity appeared to be a stronger predictor of periodontal outcomes than general obesity measured by BMI. Martínez-Herrera et al. (2017) and Khan et al. (2018) both emphasised the role of waist circumference and waist-to-hip ratio, while Kangas et al. (2017, Finland) demonstrated that adults in the highest quintile of waist circumference had a 50% higher prevalence of periodontal pockets ≥4 mm compared to those in the lowest quintile (PRR = 1.5, 95% CI: 1.2–1.9). Xu et al. (2024, China) added further evidence by reporting that android fat distribution was significantly associated with increased risk of periodontitis. Together, these results highlight the stronger predictive value of central, visceral fat measures relative to BMI. 33 Chapter 6: Discussion 6.1 Overview of Main Findings This dissertation synthesised evidence from 20 primary studies and five systematic reviews examining the association between obesity and periodontitis in adults. Across both, the direction of association was consistent: greater adiposity was linked with higher prevalence and severity of periodontal disease, though the strength varied by population, design, and metric. From the primary studies, higher BMI was generally associated with worse outcomes, including probing depth, clinical attachment loss, and CPI. National surveys and large cohorts (e.g., Kim et al., 2016; Yang et al., 2023) showed graded increases in risk across BMI categories. Central adiposity indicators such as waist circumference, waist-to-hip ratio, and waist-to-height ratio were repeatedly stronger predictors of periodontal disease than BMI, supporting the role of fat distribution. These findings corroborate earlier reviews (Keller et al., 2015; Martínez-Herrera et al., 2017; Khan et al., 2018; Kim et al., 2022). Biological plausibility was also reinforced. Elevated CRP, IL-6, and TNF-α were consistently reported in obese individuals with periodontitis (Martínez-Herrera et al., 2017; Liu et al., 2023; Harris & Rajasekar, 2024). Adipokine dysregulation, particularly reduced adiponectin and elevated leptin, further supported a mechanistic link. Some inconsistencies persisted, with smaller or heavily adjusted studies (e.g., Banihashemrad et al., 2018; Mathur et al., 2011) reporting weaker or null associations. This heterogeneity, also noted in earlier reviews, highlights the influence of methodological differences. Nonetheless, the overall evidence supports obesity particularly central adiposity as an independent risk factor for periodontitis. 6.2 Potential Mechanisms The link between obesity and periodontitis reflects multiple biological and behavioural pathways acting together. Systemic inflammation is one of the strongest explanations. Obesity is marked by elevated CRP, IL-6, and TNF-α, creating a pro-inflammatory state that may accelerate periodontal tissue destruction (Keller et al., 2015; Martínez-Herrera et al., 2017; Kim et al., 2022). Liu et al. (2023) showed that individuals with higher waist 34 circumference had both increased periodontitis and higher systemic inflammatory )2024( markers, a finding echoed by Harris & Rajasekar. Adipokine dysregulation offers another pathway. Altered secretion of leptin, adiponectin, and resistin influences immune regulation and tissue repair. Reviews (Suvan et al., 2011; Kim et al., 2022) highlighted this imbalance, while Sahar et al. (2023) observed lower adiponectin among obese adults with periodontitis. Metabolic disturbances, particularly insulin resistance, may also contribute. Obesityinduced metabolic dysfunction is associated with impaired immunity and poorer periodontal healing (Keller et al., 2015; Martínez-Herrera et al., 2017). Oxidative stress has been suggested as an additional mechanism. Excess adiposity promotes reactive oxygen species that damage periodontal tissues. Hegde et al. (2019) found higher plaque and gingival index scores among obese adults, consistent with oxidative stress. The distinction between central and general adiposity was repeatedly emphasised. Visceral fat is metabolically active, producing inflammatory cytokines more strongly linked to periodontitis. Reviews (Martínez-Herrera et al., 2017; Khan et al., 2018) and primary studies (Kangas et al., 2017; Xu et al., 2024) confirmed that waist-based measures outperformed BMI. Kangas et al. (2017) reported a 50% higher prevalence of periodontal pockets in those with the largest waist circumference. Finally, these biological mechanisms interact with social and behavioural determinants. Diets high in sugars and fats, sedentary lifestyles, low socioeconomic status, and poor access to care increase both obesity and periodontitis (Chaffee & Weston, 2010; Khan et al., 2018). Thus, the relationship is best understood as a multifactorial interplay of biological, behavioural, and structural pathways. 6.3 Methodological Issues in the Reviewed Literature The studies included in this dissertation present several methodological limitations that influence the strength and interpretation of their findings. A central limitation is the predominance of cross-sectional designs among primary studies, which restricts the ability to establish temporality or causality. This makes it unclear whether obesity precedes periodontitis, whether periodontitis exacerbates obesity, or whether both conditions share common risk determinants. Considerable heterogeneity was also observed in diagnostic criteria. Obesity was variably assessed using BMI, waist circumference, waist-to-hip ratio, or waist-toheight ratio, while definitions of periodontitis ranged from CPI and CAL thresholds to 35 more detailed case classifications. Such inconsistencies complicate comparison across studies and reduce the possibility of synthesising findings in a uniform way. Adjustment for confounders was inconsistent. While most studies accounted for age, sex, and smoking, far fewer adequately adjusted for socioeconomic status, dietary patterns, physical activity, or access to dental care factors that may strongly influence both obesity and periodontal status. Another important limitation is the underrepresentation of longitudinal evidence. Only a handful of cohort studies were available, which restricts insight into the temporal dynamics of the relationship and limits understanding of potential reverse causality. Evidence specific to adolescents and young adults was particularly scarce, with only one systematic review addressing this population (Khan et al., 2018). Finally, there was variability in study quality. Some studies used nationally representative samples and robust methodology, while others were limited by small sample sizes, narrow geographic focus, or insufficient reporting. Collectively, these methodological shortcomings highlight the need for more standardised, longitudinal, and rigorously controlled research. 6.4 Strengths and Limitations of This Dissertation This dissertation itself has several strengths. It adopted a comprehensive approach by including both primary studies and systematic reviews, enabling a broad and balanced synthesis of available evidence. The systematic search strategy, conducted in line with PRISMA guidelines, enhanced transparency and reproducibility. A further strength lies in the inclusion of central adiposity measures, such as waist circumference and waist-to-hip ratio, alongside BMI. This focus reflects growing evidence that central obesity is more biologically relevant to periodontitis risk. Moreover, the incorporation of studies from diverse global regions increased the generalisability of the findings. Nevertheless, some limitations of this dissertation must be acknowledged. As a narrative review, it did not involve meta-analysis or the calculation of pooled effect sizes, which limits the precision with which associations could be quantified. The synthesis was also constrained by heterogeneity in the definitions of both obesity and periodontitis across the included studies, reducing comparability. Furthermore, as with any review, this dissertation was dependent on the quality and availability of existing studies, the majority of which were cross-sectional, limiting the ability to assess causal relationships. Publication bias remains a possibility, since studies with null findings are less likely to be published and therefore may not have been captured. Finally, while the evidence for a bidirectional relationship between obesity and periodontitis is increasingly recognised, the included studies largely treated obesity as the exposure, restricting exploration of reciprocal pathways. 36 Taken together, these strengths and limitations provide important context for interpreting the conclusions of this dissertation. While the findings are robust in highlighting an association between obesity and periodontitis, they also point to areas where further, more rigorous research is needed. 6.5 Implications for Practice and Policy The findings of this review indicate that obesity should be considered in periodontal risk assessment, supported by consistent evidence across populations and biologically plausible mechanisms (Keller et al., 2015; Martínez-Herrera et al., 2017; Kim et al., 2022). Although causality cannot be fully established, the strength and consistency of associations justify incorporating obesity into clinical and public health strategies. In practice, dental professionals should consider simple anthropometric screening (e.g., BMI, waist circumference) as part of periodontal assessments and collaborate with medical teams to address shared risk factors. At the policy level, integrating oral health into obesity prevention programmes aligns with the Common Risk Factor Approach, as both conditions share determinants such as poor diet, smoking, and socioeconomic disadvantage. This integrated approach could maximise health promotion benefits and reduce the burden of both obesity and periodontal disease. 6.6 Implications for Future Research Future studies should prioritize longitudinal and interventional designs to better establish causality between obesity and periodontitis. Using standardized definitions for both conditions and incorporating biochemical markers such as CRP, IL-6, and TNF-α will improve comparability across studies. More research is also needed in younger populations and underrepresented regions to broaden the generalizability of findings. 6.7 Conclusion This dissertation provides consistent evidence that obesity particularly central adiposity is associated with increased risk and severity of periodontitis. 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Table 2 - Search Terms for Medline and Embase 1 obesity.mp. 2 overweight.mp. 3 BMI.mp. 4 body mass index.mp. 5 waist circumference.mp. .waist-to-hip ratio.mp 6 7 waist-to-height ratio.mp. 8 weight-adjusted waist index.mp. or 2 or 3 or 4 or 5 or 6 or 7 or 8 1 9 10 periodont*.mp. 11 periodontitis.mp. (periodont* adj3 (inflammation or pocket or .attachment loss)).mp 12 13 10 or 11 or 12 14 9 and 13 15 limit 14 to (english language and humans) 44