Protocol and registration

The review was conducted in accordance with the Arksey and O’Malley [15] framework as advanced by Levac and colleagues [16] and the Joanna Briggs Institute methodology for scoping reviews [17], and is reported in line with the PRISMA Extension for Scoping Reviews (PRISMA-ScR) [13]. The protocol was registered on the Open Science Framework (registration identifier: https://doi.org/10.17605/OSF.IO/5CW32).

Eligibility criteria

Eligibility was determined using the Population, Concept, and Context (PCC) mnemonic (Table 1). The population comprised human participants of any age residing in an African country. No age restriction was applied: although periodontitis and cardiovascular disease are predominantly diseases of adults, an inclusive criterion was adopted to avoid prematurely excluding evidence in a sparsely studied region, and the age range of included participants was charted. The concept was any reported measure of periodontal status, gingival inflammation, or periodontal treatment together with a cardiovascular or cardiometabolic outcome, surrogate, risk indicator, or a related knowledge, attitude, or care construct. A care construct was defined as any reported measure of clinician or patient knowledge, attitudes, referral practices, or service-delivery arrangements bearing on the oral-cardiovascular interface. The context included any African country and any care or community setting. Primary studies of all designs were included. Reviews, commentaries, animal and in vitro studies, and studies conducted wholly outside Africa were excluded, although global reviews were retained for background. No language or date restrictions were imposed.

Information sources and search strategy

We searched MEDLINE via PubMed, Scopus, Web of Science, and African Journals Online (AJOL) from inception to June 2026, complemented by hand-screening of the reference lists of the included studies and relevant reviews. The search combined periodontal and cardiovascular terms with an African geographic filter. A representative Boolean string for MEDLINE is as follows:

(“periodontitis” OR “periodontal disease*” OR “gingivitis” OR “clinical attachment loss” OR “periodontal pocket*”) AND (“cardiovascular disease*” OR “hypertension” OR “blood pressure” OR “atherosclerosis” OR “coronary” OR “stroke” OR “metabolic syndrome” OR “endothelial”) AND (“Africa*” OR “sub-Saharan” OR “Nigeria” OR “Cameroon” OR “Rwanda” OR “Ghana” OR “Kenya” OR “Ethiopia” OR “South Africa” OR “Egypt” OR “Tanzania” OR “Uganda” OR “Democratic Republic of Congo”).

The string was adapted to the syntax of each database. No language restriction was applied at the search stage; the practical implications of database and language coverage are addressed in the limitations.

Study selection and data charting

Two reviewers (O.G.A. and D.T.I.) independently removed duplicate records and screened them by title and abstract, followed by full-text screening. Each record was screened independently by both reviewers. Disagreements at either stage were resolved by discussion, and where consensus could not be reached, a third reviewer (A.I.O.) adjudicated. Data were charted independently by two reviewers (M.E.O. and A.B.A.) using a piloted charting form, and the completed charts were cross-checked and reconciled by the lead reviewer (O.G.A.). The charting form documented country, setting, study design, sample size, participant characteristics, the periodontal exposure definition and assessment method, the cardiovascular outcome or construct, effect estimates with confidence intervals where available, the degree of adjustment for confounders, and the authors’ main conclusions.

Synthesis of results

A meta-analysis was not conducted because of the expected variability in periodontal case definitions, outcomes, and study designs; combining data across such diverse exposure and outcome definitions would lack methodological validity [14]. The findings were synthesised using descriptive methods and categorised according to cardiovascular construct, including hypertension and blood pressure, composite cardiovascular disease, cardiometabolic risk, and constructs related to knowledge and care. In appraising causal plausibility, the findings were considered in relation to established causal viewpoints, including the consistency, strength, temporality, biological gradient, and biological plausibility of the observed associations. In line with scoping-review methodology, a formal critical appraisal of individual sources was not undertaken. Accordingly, descriptive references to study design (for example, prospective versus cross-sectional) characterise the type and limitations of the evidence and should not be read as the output of a formal quality or risk-of-bias assessment. The methodological characteristics most pertinent to interpretation, particularly study design and confounder adjustment, were charted and reported narratively [13, 17].

Selection of sources of evidence

The database and supplementary searches yielded 503 records. After removing 94 duplicates, 409 records were screened by title and abstract, resulting in the exclusion of 376 records. Subsequently, 33 full-text sources were evaluated for eligibility, with 26 excluded for the following reasons: absence of an African population (n = 11), lack of paired oral and cardiovascular measures (n = 9), and ineligible design or review article (n = 6). Ultimately, seven African primary studies satisfied the eligibility criteria and were included. Figure 1 summarizes the flow of records through identification, screening, eligibility, and inclusion.

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Figure 1. PRISMA-ScR flow of records through the scoping review. Adapted from [18]. © 2021 The Authors. Distributed under the Creative Commons Attribution (CC BY 4.0) licence.

Characteristics of sources of evidence

The included African evidence was small in volume and geographically concentrated, with most studies arising from a limited number of countries, most prominently Cameroon, Nigeria, and Rwanda, with a single additional report from Tanzania [12, 19–24]. Cross-sectional hospital- or clinic-based designs predominated, and one prospective observational study was identified [19]. Periodontal exposure was assessed inconsistently across studies using the Dutch Periodontal Screening Index, the Community Periodontal Index, full-mouth clinical attachment loss and probing depth, or composite plaque, gingival, and bleeding indices, and case definitions varied accordingly. Cardiovascular constructs ranged from physician-diagnosed cardiovascular disease and measured or self-reported hypertension to clustered cardiometabolic risk and clinician knowledge of the oral-systemic link. The principal characteristics of the included studies are summarised in Table 2. Table 2 now also reports sample size and the variables adjusted for in each study.

Three features of the evidence map are worth emphasising. First, the geographic footprint is narrow: the included studies cluster in Central, West, and East Africa, with large parts of the continent, including most of Southern Africa and the Sahel, unrepresented [12, 19–24]. Second, the design profile is shallow: with a single prospective observational exception [19], the evidence is cross-sectional and was generated in hospital or clinic populations, which limits generalisability to the community and precludes any statement about the order in which periodontal and cardiovascular changes arise. Third, exposure ascertainment is inconsistent, ranging from screening indices to full-mouth measurements, so that the same word, periodontitis, denotes materially different case definitions across studies.

Hypertension and blood pressure

Hypertension was the most frequently examined cardiovascular construct and the one for which the African evidence showed the most consistent findings. A study conducted in Rwanda among 420 adults attending two referral hospitals identified a significant association between clinical attachment loss and hypertension, with an adjusted odds ratio of 6.24 (95% CI 1.99–19.56), the strongest single estimate among the included studies; the cross-sectional design, however, precludes any inference about the temporal sequence of periodontal and blood-pressure changes [21]. In a Nigerian cardiology-clinic study, periodontal indicators correlated with elevated cardiovascular risk, including raised blood pressure, in patients already receiving cardiac care [22]. Methodologically distinct earlier research involving 81 non-smoking, non-drinking Tanzanian women not taking medication minimised confounding from antihypertensive therapy and tobacco, situating the periodontal-blood-pressure relationship within dietary factors such as potassium intake [24]. Despite substantial differences in populations and periodontal measures, the direction of the association remained consistent across these settings.

This directional consistency is reflected in the global literature. The findings agree with a systematic review and meta-analysis that identified associations between periodontitis and prevalent hypertension and higher systolic and diastolic blood pressure [7]. Combined interventional and Mendelian randomisation evidence further suggests that periodontal therapy can reduce blood pressure, indicating that this association may be the most mechanistically supported among the cardiovascular links [6]. Regional interest is evident in a systematic review led by African researchers examining oral hygiene and periodontal treatment interventions for blood pressure in low- and middle-income settings [25]. A principal caution is that the heterogeneous periodontal case definitions across the African studies preclude any consistent assessment of a dose-response gradient.

Composite cardiovascular disease and cardiometabolic risk

Beyond hypertension, the Cameroonian evidence addressed broader cardiovascular and cardiometabolic endpoints. The multi-hospital study by Belinga and colleagues, the single prospective observational design in the included set, reported associations between oral inflammatory disease and physician-diagnosed cardiovascular disease, with odds ratios of 2.87 (95% CI 1.04–7.93) for periodontitis and 4.30 (1.85–10.00) for gingivitis; the prospective element distinguishes this study from the cross-sectional remainder, although it remains observational and subject to residual confounding [19]. A study in a Cameroonian military population, an occupationally defined and relatively young group, found poorer oral health tracking with an adverse cardiovascular risk profile [20]. A third Cameroonian study related periodontal disease to newly diagnosed components of the metabolic syndrome, specifically obesity and low high-density lipoprotein cholesterol, locating the association within a cardiometabolic frame [12]. The Nigerian cardiology-clinic study similarly found periodontal indicators clustering with established cardiovascular risk factors [22]. These reports are directionally consistent with global syntheses linking periodontitis to composite cardiovascular outcomes, including incident myocardial infarction in prospective work [8, 9]. The consistency across distinct endpoints is notable in such a small body of evidence. The interpretive limitations are, however, the same throughout: with the single prospective exception, the designs are cross-sectional, the populations are hospital- or clinic-based, exposure ascertainment varies, and adjustment for shared risk factors such as smoking, diabetes, age, obesity, and socioeconomic status is frequently incomplete. The associations are therefore best read as signals warranting confirmation in stronger designs rather than as established independent effects.

Knowledge and integrated-care constructs

A distinct strand of African evidence addressed awareness and care integration rather than the association itself. A survey of Nigerian internal medicine residents found that knowledge of periodontal disease as a contributor to systemic illness was incomplete, with the oral-systemic link recognized more readily for some conditions than others, yet most respondents expressed willingness to ask about oral health and to refer patients for periodontal care if referral pathways existed [23]. The limiting factor was not clinician reluctance but a shortfall in knowledge and in the structures needed to act on it. Because physicians, rather than dentists, see most patients with cardiovascular disease in many African settings, their awareness is a rate-limiting step for any oral-systemic care pathway.

Equally notable is what the evidence map did not contain. No included study evaluated an integrated oral and cardiovascular care model, a reciprocal referral pathway, or a shared screening protocol in an African setting, and none reported patient-side knowledge, health-seeking behaviour, or barriers to accessing periodontal care alongside cardiovascular risk. This is a conspicuous gap, given that integrated dental and medical management of non-communicable disease is now recommended by international consensus [4] and that regional interest in periodontal interventions for blood pressure indicates appetite for such pathways [25].

Appraisal of causal plausibility

It must be stated plainly that causal plausibility cannot be adequately assessed from the current African evidence, which comprises seven studies that are, with one exception, cross-sectional. When the charted findings are considered against established causal viewpoints, they support compatibility with a causal link rather than causation. On consistency, the associations were consistently aligned across the included settings and with the global literature, though this is weakened by the small number of studies and the selective-reporting risks of a nascent literature [7, 21, 22]. On strength, several associations were sizeable, notably the adjusted odds ratio for clinical attachment loss and hypertension in the Rwandan study, although wide confidence intervals reflect modest samples [21]. On biological plausibility, there is supportive reasoning from mechanistic and global work; the pathways involved, including systemic inflammation, transient bacteraemia, and endothelial dysfunction, remain proposed rather than definitively established mechanisms [3, 5]. The remaining considerations are where the evidence is weakest: temporality cannot be established from cross-sectional data; a biological gradient cannot be assessed consistently because exposure is defined heterogeneously; and incomplete adjustment leaves confounding as a live alternative explanation.

This caution is echoed globally, where a large two-sample Mendelian randomisation analysis found no robust genetic support for a causal effect of periodontitis on stroke, coronary artery disease, or subclinical atherosclerosis [10]. Mendelian randomisation nonetheless warrants balanced interpretation. A null genetic finding does not exclude a causal effect, as such analyses rest on assumptions about instrument validity and may be underpowered for modest effects; conversely, the instruments are derived largely from European-ancestry genome-wide association studies, so their relevance to African populations, who differ in allele frequencies and linkage structure, is uncertain. The global genetic evidence and the African observational evidence are therefore best regarded as complementary and, at present, jointly inconclusive on causation. Presenting the contribution as one of plausibility rather than proof is the most defensible stance for a regional evidence map at this stage.

Limitations

This review has several limitations. First, only seven studies were identified, which limits the breadth and generalisability of the evidence mapped. Second, the included studies came predominantly from Cameroon, Nigeria, and Rwanda, with no representation from much of East, West, Central, and Southern Africa. Third, the evidence is overwhelmingly cross-sectional, so temporality and causality cannot be assessed. Fourth, periodontal disease was measured heterogeneously (Dutch Periodontal Screening Index, Community Periodontal Index, clinical attachment loss, and composite indices) with varying case definitions, precluding pooling. Fifth, adjustment for shared risk factors such as smoking, diabetes, and socioeconomic status was limited. Sixth, publication bias is likely, as positive associations are more readily published while negative findings may remain unpublished. Seventh, although AJOL was searched, the search relied largely on English-language databases and did not systematically interrogate other African grey-literature sources such as institutional repositories, theses and dissertations, ministry and agency reports, and conference proceedings, nor French-, Portuguese-, or Arabic-language publications; available African evidence may therefore be underestimated. Eighth, the physician-knowledge study differs qualitatively from the clinical association studies and was retained as a distinct construct within the map rather than synthesized with them. Finally, as a scoping review, this work did not assess methodological quality or perform a meta-analysis. Reference screening and the inclusion of AJOL were intended to mitigate indexing gaps, and the small yield should itself be read as a finding about the state of the evidence.

Conclusions

The association between periodontitis and cardiovascular disease in Africa is plausible and directionally supported but substantially under-evidenced. Priority research gaps are clear: population-based longitudinal studies, standardised periodontal measures, assessment of biological mechanisms in African populations, interventional studies, and health-systems research on integrated care. Despite these gaps, periodontal disease should not be neglected in cardiovascular care, given its known systemic effects, and strengthening the integration of dental and public-health services in Africa is a reasonable and low-regret step. Given the scale of both diseases on the continent, this is a priority rather than a peripheral concern.