As a Controllable Risk Factor for Cardiovascular Illnesses, Oral Health

Cardiovascular Diseases & Diagnosis

ISSN: 2329-9517

Open Access

Perspective - (2023) Volume 11, Issue 3

As a Controllable Risk Factor for Cardiovascular Illnesses, Oral Health

Serena Altamura*
*Correspondence: Department of Life, Health & Environment. Serena Altamura, Italy, Email:

Received: 02-Mar-2023, Manuscript No. jcdd-23-94016; Editor assigned: 03-Mar-2023, Pre QC No. P-94016; Reviewed: 16-Mar-2023, QC No. Q-94016; Revised: 21-Mar-2023, Manuscript No. R-94016; Published: 28-Mar-2023 , DOI: 10.37421/2329-9517.2023.11.546
Citation: Altamura, Serena. “As a Controllable Risk Factor for Cardiovascular Illnesses, Oral Health.” J Cardiovasc Dis Diagn 11 (2023): 546.
Copyright: © 2023 Altamura S. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


CVDs are a group of diseases that affect the heart and blood vessels. They are the most common non-communicable diseases and the leading cause of death and disability all over the world, with a significant impact on society and the economy. Behavioral risk factors have a significant impact on the onset and progression of cardiovascular disease (CVD), in addition to genetic factors. Unhealthy diet, inactivity, smoking, and alcohol consumption are the most important modifiable risk factors. It has been established, to the best of our knowledge that these conditions contribute significantly to the development of cardiovascular disease (CVD). Periodontal disease (PD) is a long-term, progressive inflammation of the tooth-supporting structures that eventually causes tooth loss. It is thought to be a multifactorial disease, and dysbiosis of the oral microbiome is one of the main causes [1].

Plaque buildup causes gingivitis, a reversible inflammation of the gums and soft tissues surrounding a tooth, in people who are predisposed to the condition. Whenever left untreated, gum disease advances to periodontitis, an irreversible disturbance of bone, cementum, and periodontal tendon, eventually prompting the last phase of illness, portrayed by tooth misfortune. Inflammatory mediators like interleukin-1, interleukin-6, tumor necrosis factor-, and C-reactive protein can be detected in the bloodstream as early as the onset of the disease. As the first cause of masticatory incapacity due to tooth loss and the second most common oral disease worldwide, PD has a high socioeconomic impact and affects more than half of all people. As of late, proof gathered on the side of an epidemiological relationship of this incendiary infection of the mouth with a lot of foundational medical issue, including CVDs. New evidence also indicates an independent association between PD and CVDs, in addition to sharing common denominators such as advanced age, smoking habits, male sex, low physical activity, overweight/obesity, low socioeconomic status, and poor education [2].


The biological basis for the connection between periodontal inflammation and cardiovascular disease (CVD) has been proposed to be mechanistic links, both direct and indirect. The invasion of the cardiovascular system and the transfer of proinflammatory bacteria from the oral cavity into the bloodstream are examples of direct pathways. Systemic immune pathways are triggered by indirect mechanisms, which cause and sustain chronic inflammation with possible nonspecific effects. As a result, PD has been proposed as an emerging non-traditional risk factor for CVDs that can be changed. We ask whether PD can be a modifiable risk factor for CVDs by combining the evidence from the literature in this narrative review on the mechanisms that increase cardiovascular risk in PD patients. Proof is accounted for on the inclusion of oral dysbiosis, sub-atomic and cell instruments related with irritation, and epigenetic changes as likely causal connections among PD and CVDs. Last but not least, the data on how PD treatment affects cardiovascular risk factors and diseases are discussed [3].

The connection between PD and particular cardiovascular diseases (CVDs), such as atrial fibrillation (AF), atrial fibrosis, heart failure (HF), and its various phenotypes, has been demonstrated. Specifically, the Third National Health and Nutrition Examination Survey were used in a recent study to investigate the connection between HF and periodontitis. According to the findings, people who have moderate or severe periodontitis are more likely to develop heart failure. In fact, the incidence was three times higher in the group with moderate or severe periodontitis than in the group without or with mild disease. Periodontal status was linked to adverse changes in the biomarkers of inflammation C-reactive protein and N-terminal brain natriuretic peptide as well as an increased risk for both HF with preserved ejection fraction and HF with reduced ejection fraction in the Atherosclerosis Risk in Communities Study (ARIC), which included 6707 participants and had a median follow-up time of 13 years. On the other hand, a recent study looked at how periodontitis is linked to various HF phenotypes: HF with a slightly reduced ejection fraction, HF with a preserved ejection fraction, and HF with a decreased ejection fraction [4].

Although no relevant associations were found with HF with preserved ejection fraction, severe periodontitis was found to be significantly associated with HF with mildly reduced ejection fraction. In order to explain their findings, the authors propose that PD causes systemic inflammation and vascular permeability, which in turn causes endothelial dysfunction. This, in turn, can cause myocardial ischemia and direct myocardial injury, which may be why severe PD and HF are associated with mildly reduced ejection fraction. Dental plaque and the associated acute inflammatory response may have an impact on the development of AF, as evidenced by a significant association between plaque accumulation and prevalent AF that was independent of age, sex, high-sensitivity CRP, body mass index, smoking, diabetes, and educational status. In addition, atrial fibrosis histologically analyzed in resected left atrial appendages was positively associated and correlated with all PD parameters, including oral examination, remaining teeth, bleeding on probing, periodontal probing depth, and periodontal inflamed surface area. Periodontitis is a modifiable risk factor for structural heart diseases, as demonstrated by these findings [5].

The oral microbiome is a complex community of microorganisms that live in the oral cavity and interact dynamically with the host. It includes bacteria, fungi, viruses, archaea, and protozoa. A characteristic of the onset and progression of PDs is dysbiosis of the oral microbiota. In parallel, oral dysbiosis has been linked to CVDs in increasing numbers. Bacteria and their products enter the bloodstream directly through inflamed oral tissues and indirectly through the gastrointestinal tract in patients with periodontitis, triggering systemic immune-inflammatory responses. Persistent endotoxemia, a significant cardiometabolic risk factor, has been linked to periodontitis. An increased risk of subclinical atherosclerosis, prevalent and future coronary artery disease, and incident and recurrent stroke has been linked to bacterial biomarkers of oral dysbiosis. Blood pressure profile was also found to be linked to the immunological response to periodontal bacterial. In addition, this response may also result in the production of proatherogenic antibodies that are persistent, cross-reactive, and directed against antigens derived from the host [3].

PD has been identified as an emerging modifiable non-traditional risk factor in the development and progression of cardiovascular disease (CVD) due to the significant role that inflammation plays in CVDs and the growing body of evidence linking PD to cardiovascular risk-associated biomolecular events. Oral microbiome dysbiosis, inflammatory pathways, pathogen-associated molecular patterns and damage-associated molecular patterns, pattern recognition receptors, the entero-salivary nitrate-nitrite-nitric oxide pathway, endothelial dysfunction, and epigenetic modifications are among the new elements that have been added to the framework of the mechanisms underlying the causal association between PD and CVDs. These new elements are of great interest as potential protagonists in the main the resulting image is extremely intricate and intricate. A suitable panel of PD-associated salivary or blood biomarkers that correlate with the main parameters linked to cardiovascular functions may be helpful from a diagnostic standpoint [5].


It makes sense to investigate whether periodontal treatment can aid in the management or prevention of CVD occurrence or recurrence given that evidence strongly supports a link between PD and CVDs. Many studies aimed at evaluating the effect of periodontal therapy on cardiovascular conditions are encouraging and support the causal association with CVDs, despite the fact that there are still too few randomized controlled trials to draw definitive conclusions. Controlling gum inflammation may be a biologically plausible complement to overall health, given that the inflamed area during active disease is estimated to extend to the size of a palm. For sure, late interventional and unthinking proof features an expected advantage of periodontal treatment on cardiovascular wellbeing that is to some degree interceded by its consequences for periodontal microbiome and poor quality foundational irritation.

From this point of view, periodontal therapies will be able to effectively address PD-associated systemic diseases because periodontal medicine is currently considered a novel field that collaborates with other health professions in a multidisciplinary/interdisciplinary setting. In fact, controlling overall inflammation through a good periodontal maintenance program may be able to stop or slow the progression of CVDs in people with Parkinson's disease. This model will allow, as was recently suggested, not only the prevention of numerous oral and systemic diseases that are important to the epidemiology, but also the promotion of population health and healthy lifestyles. Therefore, in the near future, it will be necessary to provide evidence that supports the necessity of integrating oral health care within health promotion strategies for oral and general wellness, given the importance of oral health for systemic wellbeing and the high prevalence of oral diseases.

Conflict of Interest





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