Background: Periodontal tissues initiate an immune-inflammatory response to bacterial invasion and their byproducts. These agents, when introduced systemically, can also trigger significant vascular reactions. Oral infection models have proven valuable in exploring the hypothesis that infections may contribute to cardiovascular disease (CVD) risk. Among these, periodontal infections are considered a primary factor, with several studies highlighting a strong association between periodontal disease and CVD. Materials and Methods: The study included 50 individuals aged between 30 and 65 years, categorized into five groups based on their diagnosed cardiovascular condition. These groups were: ischemic heart disease, bacterial endocarditis, congestive cardiac failure, valvular heart disease, and cardiomyopathies. Dental evaluations involved the use of Ramfjord’s Periodontal Disease Severity Index and assessment of clinical attachment level. Laboratory investigations included lipid profile analysis to support systemic evaluation. Observations and Results: Ramfjord’s Periodontal Disease Severity Index revealed a statistically significant difference (p < 0.05) between patients with bacterial endocarditis and those with valvular heart disease. The index also demonstrated a significant positive correlation with total cholesterol, triglycerides, and very low-density lipoproteins (VLDL), while showing a negative correlation with high-density lipoprotein (HDL). Clinical attachment level did not show significant differences between valvular heart disease and cardiomyopathies but was positively correlated with total cholesterol. The lipid profile indicated dyslipidemia in patients with ischemic heart disease.
Cardiovascular diseases (CVDs) are among the most prevalent health conditions in adults.[1,2] Common risk factors for CVD include elevated low-density lipoprotein (LDL), hypertension, smoking, male gender, and low socioeconomic status.[3,4] A potential link between infections and atherosclerotic diseases has been proposed, with several bacterial and viral agents identified as contributing factors in the development of cardiovascular conditions.[5–8]
Periodontitis and dental procedures are known to trigger transient bacteremia.[9,10] Notably, Schwartzman reactions have been reported following full-mouth debridement.[11] In patients with periodontitis, even gentle mastication can release bacterial endotoxins into the bloodstream. Additionally, oral microorganisms may enter the circulatory system from an infected root canal during or after endodontic therapy.[12]
Periodontal disease is characterized by chronic infection and inflammation of the periodontal tissues, resulting in progressive bone destruction around the teeth and eventual tooth loss.[13] In recent years, chronic infection and inflammation have increasingly been recognized as emerging risk factors in the pathogenesis of atherosclerotic cardiovascular diseases.[14,15] Although the proatherogenic role of chronic periodontal infection has yet to be conclusively established, periodontal pathogens such as Bacteroides forsythus (Tannerella forsythia), Porphyromonas gingivalis, and Prevotella intermedia have been identified in atherosclerotic plaques[16,17] as well as within coronary and aortic endothelial tissues.[18,19]
Moreover, there is growing evidence suggesting that infectious and inflammatory factors may act synergistically to elevate the risk of atherosclerotic vascular disease.[20,21] Importantly, improving oral health through periodontal treatment has been shown to positively impact the systemic and hemostatic profile of patients with coronary heart disease.[22] Therefore, individuals with heart disease represent a key population in which maintaining oral health may significantly influence overall health outcomes.
A study was undertaken to evaluate the association between periodontal disease and various forms of cardiovascular disease in patients aged 30 to 65 years, came to Government Dental College and Hospital, Paithana, Rahui, Nalanda, Bihar, India. The study spanned a duration of two months.
Study Population
A total of 50 participants were enrolled, all of whom had been diagnosed with cardiovascular disease by a cardiologist. Diagnosis was based on clinical criteria including echocardiography, treadmill test, angiography, and serum markers. All selected individuals were within the age group of 30 to 65 years.
Exclusion Criteria
Patients with the following conditions were excluded from the study:
Grouping of Participants
Participants were divided into five groups based on their specific cardiovascular diagnosis:
Data Collection and Clinical Examination
A specially designed case history proforma was used to record relevant information on each participant’s cardiovascular condition and oral health status. Ramfjord’s Periodontal Disease Severity Index was utilized to assess periodontal status in all patients.
Laboratory Investigations
Laboratory assessments included lipid profile analysis, measuring serum total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides (TG).
Statistical Analysis
Collected data were statistically analyzed using Tukey’s multiple comparison test to evaluate differences among the groups.
Figure-1 periodontal status of cardiovascular disease patients.
In the present study, 62% of the participants were diagnosed with periodontitis, while 38% exhibited gingivitis (Figure 1). Notably, none of the patients presented with a completely healthy periodontal status, indicating widespread periodontal tissue destruction among individuals with cardiovascular diseases.
Ramfjord’s Periodontal Disease Severity Index revealed statistically significant differences (p < 0.05) between patients with bacterial endocarditis and those with valvular heart disease, as well as between ischemic heart disease and valvular heart disease.
Figure-2: Plaque Component
Figure-3: Calculus Component
Plaque and calculus scores, components of the Ramfjord’s Index, were found to be relatively similar across all five cardiovascular groups. This consistency is likely due to decreased oral hygiene and plaque control as a result of prolonged hospitalization in these patients. However, the lowest scores for both plaque and calculus were observed in patients with valvular heart disease (Figures 2 and 3).
Figure-4: Gingival and periodontal
Figure-5: Correlation of gingival
When examining the gingival and periodontal components of Ramfjord’s Index in relation to lipid profiles, the highest mean scores were noted in patients with ischemic heart disease, followed by bacterial endocarditis. The lowest scores were recorded in patients with valvular heart disease (Figure 4).
Furthermore, both the gingival and periodontal components of Ramfjord’s Index demonstrated a significant positive correlation with total cholesterol, triglycerides, and very low-density lipoproteins (VLDL), and a negative correlation with high-density lipoprotein (HDL) (Figure 5).
Figure-6: Clinical Attachment Level
Figure7: Correlation of Clinical Attachment
Regarding clinical attachment levels, the highest mean values were again associated with ischemic heart disease, while the lowest (non-significant) scores were observed in patients with valvular heart disease and cardiomyopathies (Figures 6 and 7). A positive correlation was found between clinical attachment level and total cholesterol level. This may be attributed to the extensive periodontal destruction in ischemic heart disease and bacterial endocarditis, potentially due to increased bacteremia, vasoconstriction, and reduced blood supply resulting from bacterial endotoxins.
Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality worldwide, despite significant advancements in understanding their pathogenesis and treatment. Among the most common conditions are coronary heart disease (CHD) and bacterial endocarditis. CHD is widely recognized as a multifactorial disease, with several studies reporting associations with gram-negative bacteria (e.g., Helicobacter pylori, Chlamydiae pneumoniae) and viruses such as cytomegalovirus.
In recent years, inflammation has emerged as a central factor in the pathogenesis of cardiovascular diseases. Chronic dental infections, particularly periodontitis, have been proposed as potential contributors to systemic inflammation and CHD. Periodontitis is characterized by chronic infection and inflammation of the periodontal tissues, capable of inducing a systemic inflammatory response, as evidenced by elevated C-reactive protein (CRP) levels. Transient bacteremia caused by periodontal infections may facilitate the dissemination of pathogens into atherosclerotic plaques, promoting inflammation and plaque instability—potentially triggering ischemic events.
To reduce the influence of confounding factors, the present study excluded individuals with smoking habits and diabetes, both of which are established risk factors for heart disease and periodontitis. The age range of 30 to 65 years was selected to capture early-onset CVD while minimizing age-related physiological biases that may affect results. This age range is consistent with prior studies, including those by Miyaki K, Lopez R, and Cueto A [25–27].
A male predominance (62% male vs. 38% female) was observed in our study, aligning with global data suggesting that men are more prone to coronary heart disease, stroke, and other cardiovascular conditions. The exact reasons remain unclear, though the protective role of estrogen in females is widely recognized as a significant factor.
Recent research has suggested a link between periodontitis and hypertension, though findings remain inconclusive [30]. In our study, a significant proportion of participants reported a history of hypertension, consistent with observations by Lopez R, Cueto A, and Stein JM [26,27,31].
Cholesterol levels, particularly high total cholesterol and triglycerides, are well-established predictors of CHD. Periodontitis has been associated with increased levels of pro-atherogenic lipoproteins. Chronic low-level exposure to gram-negative bacterial lipopolysaccharides (LPS) can alter lipid metabolism, often leading to hypertriglyceridemia and lipid oxidation via inflammatory mediators such as TNF-α and IL-1β.
In the present study, 30 out of 50 participants had a documented history of hypercholesterolemia, with 30 individuals presenting triglyceride levels exceeding the recommended threshold of 150 mg/dL. This association was statistically significant and aligned with findings from studies by Cueto A and Miyaki K [25,27,32], though some contrasting results have been reported [31,33].
Poor periodontal health was prevalent among heart disease patients in this study. Similar findings have been reported in other investigations [27,29]. Both periodontal and cardiovascular diseases share common inflammatory pathways and cellular mediators, including monocytes, lymphocytes, polymorphonuclear leukocytes, fibroblasts, and endothelial cells. Notably, epithelial cells and osteoblasts contribute to inflammation in periodontitis, whereas smooth muscle cells play a similar role in CVD.
A key pathological feature shared by both diseases is the degradation of connective tissue—particularly collagen—mediated by matrix metalloproteinases (MMPs). In periodontitis, MMPs break down periodontal connective tissue, leading to tooth loss. In atherosclerosis, MMPs degrade the fibrous cap of plaques, increasing the risk of myocardial infarction.
Biologically plausible mechanisms have been proposed to explain the link between periodontal and cardiovascular diseases. For instance, Streptococcus sanguis has been shown to promote platelet aggregation and thrombus formation, potentially contributing to myocardial infarction. Additionally, pathogens such as Porphyromonas gingivalis and S. sanguis have been isolated from atherosclerotic plaques [18,19].
MMPs play a significant role in both periodontal destruction and the pathophysiology of cardiovascular conditions, including heart failure. Emerging evidence suggests that MMP inhibitors, proven effective in preventing periodontal attachment loss, may also be beneficial in managing cardiovascular conditions by mitigating extracellular matrix degradation in the myocardium.
The findings of this study suggest a significant association between periodontitis and cardiovascular diseases. This relationship remained strong even after controlling for conventional risk factors such as smoking, diabetes, and age. The results further reinforce the growing body of evidence that chronic inflammatory conditions—particularly periodontal disease—may play a contributory role in the pathogenesis of heart diseases. These observations highlight the importance of maintaining good oral health not only for dental well-being but also as a potential preventive measure for cardiovascular complications.