Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

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On Sep 2018

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"Journal of Clinical and Diagnostic Research is at present a well-known Indian originated scientific journal which started with a humble beginning. I have been associated with this journal since many years. I appreciate the Editor, Dr. Hemant Jain, for his constant effort in bringing up this journal to the present status right from the scratch. The journal is multidisciplinary. It encourages in publishing the scientific articles from postgraduates and also the beginners who start their career. At the same time the journal also caters for the high quality articles from specialty and super-specialty researchers. Hence it provides a platform for the scientist and researchers to publish. The other aspect of it is, the readers get the information regarding the most recent developments in science which can be used for teaching, research, treating patients and to some extent take preventive measures against certain diseases. The journal is contributing immensely to the society at national and international level."

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Sanjay Gandhi institute of trauma and orthopedics,
On Aug 2018

Dr. Mamta Gupta,
"It gives me great pleasure to be associated with JCDR, since last 2-3 years. Since then I have authored, co-authored and reviewed about 25 articles in JCDR. I thank JCDR for giving me an opportunity to improve my own skills as an author and a reviewer.
It 's a multispecialty journal, publishing high quality articles. It gives a platform to the authors to publish their research work which can be available for everyone across the globe to read. The best thing about JCDR is that the full articles of all medical specialties are available as pdf/html for reading free of cost or without institutional subscription, which is not there for other journals. For those who have problem in writing manuscript or do statistical work, JCDR comes for their rescue.
The journal has a monthly publication and the articles are published quite fast. In time compared to other journals. The on-line first publication is also a great advantage and facility to review one's own articles before going to print. The response to any query and permission if required, is quite fast; this is quite commendable. I have a very good experience about seeking quick permission for quoting a photograph (Fig.) from a JCDR article for my chapter authored in an E book. I never thought it would be so easy. No hassles.
Reviewing articles is no less a pain staking process and requires in depth perception, knowledge about the topic for review. It requires time and concentration, yet I enjoy doing it. The JCDR website especially for the reviewers is quite user friendly. My suggestions for improving the journal is, more strict review process, so that only high quality articles are published. I find a a good number of articles in Obst. Gynae, hence, a new journal for this specialty titled JCDR-OG can be started. May be a bimonthly or quarterly publication to begin with. Only selected articles should find a place in it.
An yearly reward for the best article authored can also incentivize the authors. Though the process of finding the best article will be not be very easy. I do not know how reviewing process can be improved. If an article is being reviewed by two reviewers, then opinion of one can be communicated to the other or the final opinion of the editor can be communicated to the reviewer if requested for. This will help one’s reviewing skills.
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Dr. Mamta Gupta
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Aug 2018

Dr. Rajendra Kumar Ghritlaharey

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Salient features of the JCDR: It is a biomedical, multidisciplinary (including all medical and dental specialities), e-journal, with wide scope and extensive author support. At the same time, a free text of manuscript is available in HTML and PDF format. There is fast growing authorship and readership with JCDR as this can be judged by the number of articles published in it i e; in Feb 2007 of its first issue, it contained 5 articles only, and now in its recent volume published in April 2011, it contained 67 manuscripts. This e-journal is fulfilling the commitments and objectives sincerely, (as stated by Editor-in-chief in his preface to first edition) i e; to encourage physicians through the internet, especially from the developing countries who witness a spectrum of disease and acquire a wealth of knowledge to publish their experiences to benefit the medical community in patients care. I also feel that many of us have work of substance, newer ideas, adequate clinical materials but poor in medical writing and hesitation to submit the work and need help. JCDR provides authors help in this regards.
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Indexation and online availability: Indexation transforms the journal in some sense from its local ownership to the worldwide professional community and to the public.JCDR is indexed with Embase & EMbiology, Google Scholar, Index Copernicus, Chemical Abstracts Service, Journal seek Database, Indian Science Abstracts, to name few of them. Manuscriptspublished in JCDR are available on major search engines ie; google, yahoo, msn.
In the era of fast growing newer technologies, and in computer and internet friendly environment the manuscripts preparation, submission, review, revision, etc and all can be done and checked with a click from all corer of the world, at any time. Of course there is always a scope for improvement in every field and none is perfect. To progress, one needs to identify the areas of one's weakness and to strengthen them.
It is well said that "happy beginning is half done" and it fits perfectly with JCDR. It has grown considerably and I feel it has already grown up from its infancy to adolescence, achieving the status of standard online e-journal form Indian continent since its inception in Feb 2007. This had been made possible due to the efforts and the hard work put in it. The way the JCDR is improving with every new volume, with good quality original manuscripts, makes it a quality journal for readers. I must thank and congratulate Dr Hemant Jain, Editor-in-Chief JCDR and his team for their sincere efforts, dedication, and determination for making JCDR a fast growing journal.
Every one of us: authors, reviewers, editors, and publisher are responsible for enhancing the stature of the journal. I wish for a great success for JCDR."

Thanking you
With sincere regards
Dr. Rajendra Kumar Ghritlaharey, M.S., M. Ch., FAIS
Associate Professor,
Department of Paediatric Surgery, Gandhi Medical College & Associated
Kamla Nehru & Hamidia Hospitals Bhopal, Madhya Pradesh 462 001 (India)
On May 11,2011

Dr. Shankar P.R.

"On looking back through my Gmail archives after being requested by the journal to write a short editorial about my experiences of publishing with the Journal of Clinical and Diagnostic Research (JCDR), I came across an e-mail from Dr. Hemant Jain, Editor, in March 2007, which introduced the new electronic journal. The main features of the journal which were outlined in the e-mail were extensive author support, cash rewards, the peer review process, and other salient features of the journal.
Over a span of over four years, we (I and my colleagues) have published around 25 articles in the journal. In this editorial, I plan to briefly discuss my experiences of publishing with JCDR and the strengths of the journal and to finally address the areas for improvement.
My experiences of publishing with JCDR: Overall, my experiences of publishing withJCDR have been positive. The best point about the journal is that it responds to queries from the author. This may seem to be simple and not too much to ask for, but unfortunately, many journals in the subcontinent and from many developing countries do not respond or they respond with a long delay to the queries from the authors 1. The reasons could be many, including lack of optimal secretarial and other support. Another problem with many journals is the slowness of the review process. Editorial processing and peer review can take anywhere between a year to two years with some journals. Also, some journals do not keep the contributors informed about the progress of the review process. Due to the long review process, the articles can lose their relevance and topicality. A major benefit with JCDR is the timeliness and promptness of its response. In Dr Jain's e-mail which was sent to me in 2007, before the introduction of the Pre-publishing system, he had stated that he had received my submission and that he would get back to me within seven days and he did!
Most of the manuscripts are published within 3 to 4 months of their submission if they are found to be suitable after the review process. JCDR is published bimonthly and the accepted articles were usually published in the next issue. Recently, due to the increased volume of the submissions, the review process has become slower and it ?? Section can take from 4 to 6 months for the articles to be reviewed. The journal has an extensive author support system and it has recently introduced a paid expedited review process. The journal also mentions the average time for processing the manuscript under different submission systems - regular submission and expedited review.
Strengths of the journal: The journal has an online first facility in which the accepted manuscripts may be published on the website before being included in a regular issue of the journal. This cuts down the time between their acceptance and the publication. The journal is indexed in many databases, though not in PubMed. The editorial board should now take steps to index the journal in PubMed. The journal has a system of notifying readers through e-mail when a new issue is released. Also, the articles are available in both the HTML and the PDF formats. I especially like the new and colorful page format of the journal. Also, the access statistics of the articles are available. The prepublication and the manuscript tracking system are also helpful for the authors.
Areas for improvement: In certain cases, I felt that the peer review process of the manuscripts was not up to international standards and that it should be strengthened. Also, the number of manuscripts in an issue is high and it may be difficult for readers to go through all of them. The journal can consider tightening of the peer review process and increasing the quality standards for the acceptance of the manuscripts. I faced occasional problems with the online manuscript submission (Pre-publishing) system, which have to be addressed.
Overall, the publishing process with JCDR has been smooth, quick and relatively hassle free and I can recommend other authors to consider the journal as an outlet for their work."

Dr. P. Ravi Shankar
KIST Medical College, P.O. Box 14142, Kathmandu, Nepal.
On April 2011

Dear team JCDR, I would like to thank you for the very professional and polite service provided by everyone at JCDR. While i have been in the field of writing and editing for sometime, this has been my first attempt in publishing a scientific paper.Thank you for hand-holding me through the process.

Dr. Anuradha
On Jan 2020

Important Notice

Year : 2022 | Month : October | Volume : 16 | Issue : 10 | Page : ZE01 - ZE06 Full Version

Contemporary Consortium of Periodontal Diseases and Atherosclerotic Cardiovascular Diseases- A Narrative Review

Published: October 1, 2022 | DOI:
Roshan R Rughwani, Priyanka K Cholan, Dhayanand John Victor

1. Postgraduate, Department of Periodontics, SRM Dental College, Ramapuram, Chennai, Tamil Nadu, India. 2. Associate Professor, Department of Periodontics, SRM Dental College, Ramapuram, Chennai, Tamil Nadu, India. 3. Professor and Head, Department of Periodontics, SRM Dental College, Ramapuram, Chennai, Tamil Nadu, India.

Correspondence Address :
Dr. Roshan R Rughwani,
2F, Poonam Apartments, No-66 Old No.- 80, MG Road, Nungambakkam, Chennai, Tamil Nadu, India.


Periodontal medicine unravels the relationship between periodontal health and disease with systemic health and disease. Periodontal disease serves as a niche for abundant quantity of microorganisms and their byproducts that disseminate into the blood stream. This systemic spread of endotoxins is directly related to the amount of periodontal destruction occurring at any given point of time and is responsible for bridging the link between inflammatory periodontal disease and various other systemic diseases. It is a well-known fact that periodontal diseases have been linked to various systemic diseases including osteoporosis, kidney diseases, adverse pregnancy outcomes, diabetes and even atherosclerotic cardiovascular diseases. Both periodontal diseases and atherosclerotic cardiovascular diseases share the same risk factors. Although both the diseases are multifactorial, the complex pathogenic mechanism orchestrating periodontal and atherosclerotic cardiovascular diseases share a considerate portion of the proinflammatory trait and several biochemical mediators play a role in the pathogenesis and inflammatory response in periodontitis caused by bacterial infections, linking chronic periodontitis to atherosclerotic cardiovascular disease. This review focuses on enlightening the plausible mechanisms that link periodontal and cardiovascular diseases and highlights the various other aspects of periodontal medicine that establishes a two-way relationship between periodontal diseases and atherosclerotic cardiovascular diseases. Understanding the nature of this association would ultimately aid clinicians to carefully plan treatment for patients and emphasise the importance of maintaining optimal oral hygiene in atherosclerotic patients in a more comprehensive and acceptable manner.


Association, Bacteraemia, Bidirectional link, Inflammation, Immune modulation, Periodontitis, Hyperlipidaemia, Periodontal medicine

Periodontal disease is a chronic inflammatory disease that is initiated by a dysbiotic microbiome in the gingival sulcus which activates the immune response through an array of host cell-based receptors that initiate intra and intercellular signalling, thereby further activating the host immune-inflammatory response (1). It is the sixth most common disease affecting the general population and is characterised by surface proteins and endotoxins such as the Lipopolysaccharides (LPS), that instigate the production of various proinflammatory cytokines which get involved in tissue destruction through the release of other mediators such as Matrix-Metalloproteinases (MMPs), prostaglandins, leukotrienes, nitrogen and oxygen derived free radicals through a cascading series of events initiated by the dysbiotic microflora (2). These events link periodontal disease to various systemic diseases including cardiovascular diseases, osteoporosis, kidney diseases, adverse pregnancy outcomes, and diabetes. Since, both periodontal diseases and atherosclerotic cardiovascular diseases share the same risk factors and are multifactorial in nature, the existence of common complex pathogenic mechanism orchestrating periodontal and cardiovascular diseases contribute to a considerate portion of the inflammatory component (3). This narrative review focuses on indoctrinating the plausible mechanisms that link periodontal and atherosclerotic cardiovascular diseases and highlights the various other aspects of periodontal medicine that establishes a two-way relationship between periodontal diseases and atherosclerosis.


The usual symbiotic interaction between the host and the pathogen is dysregulated in periodontitis due to the abundance of pathogens in the biofilm and their virulence factors, which causes an exaggeration in the host immune response. This dysbiotic microflora’s creation of a dangerous microenvironment causes an immunological reaction that is particularly prominent where the biofilm is located, which causes exponential damage to the periodontal tissues and is the primary trigger for the transformation of gingivitis into periodontitis (4). A wide range of chemical mediators, including interleukins and prostaglandins, are produced when phagocytes like neutrophils and macrophages transmigrate to the site of bacterial insult. These mediators not only help to maintain local inflammation but also help to signal inflammatory cells to move closer to the site of periodontal destruction. These phagocytic cells have Toll-like Receptors (TLRs) on their surface that are capable of recognising Pathogen-associated Molecular Patterns (PAMPs). This triggers a series of events through the MyD88-dependent pathway that causes the production of Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), which regulates the release of proinflammatory cytokines like Interleukin 1 (IL-1), Tumour Necrosis Factor (TNF) and Interleukin 6 (IL-6) (5).

First, phagocytes like neutrophils and macrophages transmigrate to the site of the bacterial insult, where they release a variety of chemical mediators like interleukins and prostaglandins that not only help to maintain the localised inflammatory response but also help signal inflammatory cells to move closer to the site of periodontal damage. These phagocytic cells have TLRs on their surfaces that are trained to detect PAMPs, or pathogen-associated molecular patterns. This triggers a series of events through the MyD88-dependent pathway that renders the production of NF-κB, which regulates the release of proinflammatory cytokines.


Atherosclerotic cardiovascular disease is a lipid storage disorder that is characterised by the deposition of lipid-rich substances in the subendothelial connective tissue of vasculature that supplies the heart, brain and other peripheral organs. It is the underlying cause of almost 50% of the mortality in the western world, and is characterised by focal thickening of the vasculature in response to an immune reaction that internalises the circulating lipids by a complex mechanism that activates the vascular endothelium and the vascular smooth muscle cells (6),(7). Although the aetiopathogenesis of atherosclerosis is not clear, studies show that the major risk factors for atherosclerosis are obesity, diabetes, smoking and hyperlipidaemia.

Hyperlipidaemia, is the most important and validated risk factor for atherosclerosis, that is characterised by lipid accumulation in the vascular sub-endothelial spaces, which triggers an inflammatory response. Low Density Lipoprotein (LDL) also get trapped in the sub-endothelial layers of the artery by the binding of proteoglycans in the subendothelial connective tissue and the apoB present in the LDL (8). These accumulated LDL molecules spontaneously undergo oxidation when it comes in contact with the ROS, generated by the macrophages and the endothelial cells which act as a ligand for the TLR2 surface receptor of the macrophages thereby directly triggering the proinflammatory signalling pathways (9). This further enhances the activity of the inflammatory cells which is directly related to the coronary plaque accumulation consisting of a central lipid core surrounded by a layer of lipid laden macrophages (foam cells) and a collagenous cap encasing it. There is moderate strength of association between periodontitis and Atherosclerotic Cardiovascular Diseases (ACVD) as reported by many studies that have used to evaluate different surrogate measures such as endothelial function and C-Reactive Protein (CRP) levels (10). The elevated levels of inflammatory cytokines are present during both periodontitis and cardiovascular disease, and several biologically plausible mechanisms have been demonstrated in previous studies which are in coherence with numerous animal and human studies thereby proving that an association exists between periodontal disease and cardiovascular disease (11).


It is fascinating to know that several possible direct and indirect mechanisms may operate independently or synchronously to explain the association between periodontal diseases and atherosclerotic cardiovascular diseases (12).

Direct Mechanism

Direct bacterial Invasion: This mechanism involves the direct invasion of the periodontal microorganism into the endothelial cells. Pathogens present in the periodontal pockets are frequently present in the systemic circulation which may get localised to atherosclerotic lesions (13). Marcelino SL et al., showed the presence of common periodontal pathogens like Prevotella intermedia, Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans and Tannerella forsythus by real time Polymerase Chain Reaction (PCR) method in atherosclerotic plaque samples of patients having periodontal disease (14). Another study also suggests that atherosclerotic lesions harbour periodontal pathogens which enter the blood stream directly to reach the atheromatous tissues (15).

Streptococcus sanguis, a commensal of the oral cavity, is the most frequently isolated organism in dental plaque including sub gingival sites. While not considered to be a periodontal pathogen, this organism enters the circulation by contact with chronically inflamed and ulcerated periodontal tissues. In severe periodontitis the complex bacterial plaque can be exposed to wounded gingiva with a surface area of up to 50 cm2. Surface fibrils expressed by certain strains of S.sanguis cause human platelets in plasma to agglutinate in-vitro. These fibril proteins have been directly implicated in the development of thrombi and the growth of experimental endocarditis in-vivo (16).

Porphyromonas gingivalis demonstrates the aggregate (Agg+) phenotype and a PAAP cross-reactive antigen, in addition to S. sanguis. Herzberg MC and Weyer MW, reported that Porphyromonas gingivalis possess properties similar to that of Streptococcus sanguis. If the Agg+ phenotype is thrombogenic, one could speculate that P. gingivalis as a putative periodontal pathogen may contribute to both the chronic lipopolysaccaride mediated and Agg+ mediated pathways to atherosclerosis and thrombosis (17). Also Fusobacterium nucleatum and T. forsythia may work together to help P. gingivalis invade endothelial cells (18),(19). It was further reported that Matrix Metalloproteinase-2 (MMP-2) expression in the interstitial tissues increased significantly due to Aggregatibacter actinomycetemcomitans infection (20). Thus periodontal pathogens are present in atherosclerotic plaques and may play a role in the development and progression of atherosclerosis leading to coronary artery disease and other clinical sequalae (21).

Indirect bacterial spread: In addition to this direct spread, pathogens may also invade the phagocytic cells and the ability of them to survive within the phagocytes (Trojan Horse approach) may allow them to reach anatomically distant sites. Another mechanism by which a dormant Porphyromonas gingivalis of the periodontium may reach distant sites, is by modulating the cellular machinery wherein they multiply within the epithelial cells and later gain access to the vasculo-endothelial system (21). Once internalised, the periodontal pathogens causes the endothelium to dysfunction which could be seen as a potential association between reduced salivary nitric oxide level and endothelial dysfunction in periodontitis patients (22).

Monocyte-response to bacterial challenge - the ultimate regulator of periodontal disease expression: The important proinflammatory mediators - Prostaglandin E2 (PGE2), IL-1β, and TNFα -are secreted by the monocyte within the periodontium in response to the bacterial LPS from periodontal infections. By causing vasodilatation, increasing vasopermeability, inflammatory cell recruitment, connective tissue degradation, and alveolar bone disintegration, these mediators in turn have detrimental effects on the periodontium. Normal M2 anti-inflammatory phenotype people often exude less of these mediators in response to LPS in culture against M1 proinflammatory phenotype individuals (23).

Both atheroma development and periodontal disease are significantly aided by cells of the monocytic lineage and the accompanying cytokines. A systemic hyper inflammatory monocyte phenotype, which secretes abnormally high quantities of inflammatory cytokines, is seen in many individuals with severe types of periodontal disease and insulin dependent diabetes mellitus. This suggests that the underlying M1 phenotype may put a patient at risk for developing atherosclerosis and emboli (24).

These mechanisms depict that periodontal disease increases the systemic inflammatory burden and that the oral pathobionts, which are commonly found in circulation and in atherosclerotic tissues, are efficient enough to promote inflammation.

Indirect Mechanism

Role of LPS and bacterial byproducts: Recent research has demonstrated that bacteraemia not only causes the engagement of periodontal pathogens or their byproducts (lipopolysaccharide) in the liver, which activates systemic inflammatory mediators, but also direct seeding of periodontal pathogens in atheromas, providing a second mechanism by which periodontal diseases may promote atherosclerotic cardiovascular diseases. Lipopolysaccharides are released as extracellular blebs from microorganisms within the periodontal pocket and may enter the diseased periodontium. Intravascular infusion of LPS induces platelet adhesion and aggregation by the release IL-1β, TNF-α, and Thromboxane B2 (TxB2) which increases the expression of endothelial adhesion molecules, and encourages the growth of cholesterol-rich foam cells and intimal cholesterol deposition (25).

Kuramitsu HK et al., showed that the outer membrane vesicles of P. gingivalis was able to induce foam cell formation in a model system using human umbilical vein endothelial cells and the murine macrophage cell line J774 A1 (26). This property appeared to be mediated by the Lipopolysaccharide (LPS) fraction of the cells. The ability of P. gingivalis to interact with endothelial cells which triggers the synthesis of Monocyte Chemo-attractant Protein-1 has been suggested (27). This enhanced the recruitment of circulating monocytes to these sites.

Since, the rupture of the fibrous cap of plaque appears to be a key role in acute coronary syndrome, P. gingivalis 381 was found to disintegrate fibrous caps isolated from autopsy samples. Furthermore, strain 381 substantially enhanced MMP-9 protease activity, which has been linked to plaque rupture. These literature findings elicit that P. gingivalis exhibits several properties, which may play a role in foam cell formation and rupture of atherosclerotic plaque. Thus LPS as a systemic trigger can activate an impressive cascade of inflammatory cytokines, which are capable of eliciting most of the vascular, and coagulation complications associated with atherosclerosis.

Role of fibrinogen and white blood cell: In the literature it has been consistently reported that the presence of periodontal disease leads to an increased fibrinogen level and White Blood Cell (WBC) count thereby having direct impact on the blood rheology by increasing its viscosity (28).

Increased likelihood of thrombus formation may be seen as a consequence of increased blood viscosity that may encourage atherogenesis and thrombogenesis. The most significant contributor to the promotion of hypercoagulable condition is likely fibrinogen. Increased amounts cause blood viscosity since it is the precursor of fibrin, a crucial factor in platelet aggregation (29).

Elevated white blood cell count is also a predictor of heart disease and stroke and circulating leucocytes may promote occlusion of blood vessels and several authors have enlisted increased WBC as a risk factor for development of ACVD (30).

Role of C-reactive protein: C-reactive protein levels that are moderately high have been linked to an increased risk of myocardial infarction, stroke, and symptoms of peripheral artery disease in the future. It is shown to enhance LDL aggregation and production of Vascular Cell Adhesion Molecule-1 (VCAM-1) in endothelial cells (31). Macrophages readily take up LDL bound to immobilised CRP aggregates and this uptake induces the expression of adipophillin, a specific marker of cholesterol-laden macrophages (32).

For CRP to be involved in the formation of foam cells it is necessary that this protein aggregates and binds to LDL molecules. Such aggregation occurs by a calcium dependent process. Despite the fact that CRP is a general indicator of inflammation, studies show that it is high in periodontal disease, which accelerates the development of atherosclerosis by binding to LDL and forming unstable plaque (33).

Role of other systemic inflammatory mediators: Periodontitis is known to emanate systemic biomarkers such as the CRP, LDL, TNFα, IL6 and IL1β that cause endothelial dysfunction and dyslipidaemia (34).

It has been well-recognised that inflammation induces marked changes in lipid metabolism which can be conveniently associated to the raised levels of an array of systemic inflammatory markers, predominantly CRP, IL1β, TNFα, and IL6. (Table/Fig 1) (27),(35),(36),(37),(38),(39),(40),(41),(42),(43).

Role of heat-shock proteins: Recently is has been suggested that antibodies expressed by patients with periodontitis could also promote atheroma formation through the mechanism of ‘molecular mimicry’. In patients with atherosclerosis compared to healthy controls, antibody levels to Porphyromonas gingivalis HSP60s were found to be higher, which suggested that Heat Shock Protein 60 was one such molecule that may be involved in the pathogenesis of both atherosclerosis and chronic periodontitis (44). HSPs may have a significant pathogenic role in subgingival plaque as Chung SW et al., demonstrated elevated humoral immune response to HSP-60 family in periodontitis patients (45). Antibodies against P. gingivalis, Fusobacterium nucleatum and human HSP were found in the sera and inflamed gingival tissues of periodontitis patients (46). Further, HSP-60 in Actinobacillus actinomycetemcomitans is a potent bone-resorbing mediator. High levels of HSP-60 are stimulated by persistent oral infections in those at cardiovascular risk. There is a chance of an autoimmune reaction on the surface of the vessel if antibodies made against bacterial HSP interact with HSPs generated in the host tissue, particularly if they are located in the lining of blood vessels. In the presence of a risk factor, this might start a chain of host reactions that could lead to the development of atheromatous lesions (47).

Hence, it can be suggested that inspite of the presence of various confounding variables, periodontal disease is an independent risk factor which increases the likelihood for the initiation and progression of ACVD (3).


Elevated levels of inflammatory cytokines are present during both periodontitis and ACVD, and the aforementioned plausible mechanisms that have also been reported in previous studies are in coherence with previous animal and human data which explain the association of both the multifactorial diseases (Table/Fig 2) (4),(5),(8),(11).

As evidence persisted indicating periodontitis was a significant risk factor for cardiovascular pathology in susceptible individuals, the term Periodontitis-Atherosclerosis Syndrome (PAS) was introduced as a diagnostic terminology to represent persons with both periodontal disease and ACVD (48).

Various controlled trials and reviews have established periodontal disease to be an independent risk factor for development of ACVD. The literature has been surrounded with many studies examining the strength of the link between periodontitis and cardiovascular diseases and its biological plausibility ever since Mattile KJ, initially reported on the association between Cardiovascular Disease (CVD) and oral infections in 1989 (49). Since then, ACVD and periodontal disease have been linked in several epidemiological studies. Sanz M et al., reported that the higher prevalence of subclinical atherosclerosis was associated with increased periodontal probing depth and clinical attachment loss (50). Nordendahl E et al., reported an increased risk for MI in female periodontitis subjects aged below 65 years by reporting an odds ratio of 3.72 while correlating the probing depth, bleeding on probing and alveolar bone loss to the first MI (51). Górski B et al., also reported an odds ratio of 2.4 while correlating the similar periodontal parameters to the incidence of MI (52). Dietrich T et al., reported a hazard ratio of 2.12 while correlating the probing depth and alveolar bone loss to the risk of developing fatal cardiovascular events (53). A recent meta-analysis has reported that decreased number of teeth confers to a greater risk of development of ACVD and mortality, while, other meta-analyses have consistently concluded that the available evidence indicates that periodontal diseases confer a moderate risk for atherosclerosis and its consequences (54),(55).

These evidences show that there is a bidirectional association between two common inflammatory conditions- periodontitis and ACVD, where in the common denominator between the diseases is bacteraemia and the inflammatory trait and that periodontitis poses a moderate risk of development of ACVD.

Does Periodontal Treatment Reduce the Risk of Initiation and Progression of ACVD?

Periodontal therapy consists of mechanical debridement of root surfaces and elimination of biofilm. Patients treated by non surgical periodontal therapy displayed a significant increase in plasma TNFα, CRP, and IL-6 levels immediately after intervention measured by Enzyme Linked Immunosorbent Assay (ELISA), which suggests a systemic acute phase response, possibly caused by massive bacterial inoculation in conjunction with the instrumentation of periodontal tissue (56).

A systemic review of six treatment studies investigating the effects of non surgical periodontal therapy or serum CRP levels concluded that there is modest evidence of a treatment-induced reduction in CRP (57). A recent systematic review by Teeuw WJ et al., also suggested that non-surgical periodontal therapy reduced the risk of ACVD by decreasing the levels of proinflammatory and thrombotic markers showing a significant Weighted Mean Difference (WMD) for CRP, IL-6, TNF-α, fibrinogen, total cholesterol and High-Density Lipoprotein (HDL) Cholesterol favouring periodontal treatment (58).

Several studies and randomised clinical trials have reported improvement of endothelial function and associated markers of inflammation among subjects with periodontitis who have undergone non surgical periodontal therapy with or without systemic antibiotic (59),(60). A landmark study by Bokhari SAH et al., suggested that non surgical periodontal therapy was successful in reducing the levels of CRP, fibrinogen and WBCs in cardiac patients (33).

The effect of surgical periodontal therapy on the improvement of cardiovascular risk markers were reported by Gupta B et al., where in, a decrease in the CRP level three months after completion of surgical periodontal therapy (61). While, Moeintaghavi A et al., reported a decrease in all lipid profile parameters excepting HDL after three months of completion of surgical periodontal therapy (62).

Evidences related to the adjunctive use of antibiotics in addition to non surgical periodontal therapy also claim them to be beneficial as Jockel-Schneider Y et al., (63) who reported a greater decrease in the pulse-wave velocity at the end of 12 months in a group of subjects who were given amoxicillin (500 mg) and metronidazole (400 mg) as an adjunct to non surgical periodontal therapy. Montero E et al., reported a greater decrease in CRP and fibrinogen level after completion of non surgical periodontal therapy and adjunctive antibiotic treatment (60).

With these data it can be suggested that periodontal therapy not only reduces the levels of inflammatory markers for a short duration of time, but it also has long-term effects on the levels of these systemic inflammatory markers.


Although periodontitis is an independent risk factor of ACVD, it still remains a complicated task to diagnose and treat an ACVD patient periodontally and to map its routes to poor periodontal health. Thereby, emphasising the significance of comprehending the reciprocal relationship between periodontitis and ACVD. Further, concept of minimising deleterious effects of periodontal disease on the progression of ACVD also represents an unprecedented challenge to the dental fraternity. Time is not far away when periodontists will work in unison with cardiovascular physicians and surgeons in crucial decision making and deliver optimal dental and medical treatment to patients ailing with cardiac diseases in a comprehensive and a sophisticated manner.


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DOI and Others

DOI: 10.7860/JCDR/2022/57367.16893

Date of Submission: Apr 27, 2022
Date of Peer Review: May 21, 2022
Date of Acceptance: Jun 29, 2022
Date of Publishing: Oct 01, 2022

• Financial or Other Competing Interests: None
• Was Ethics Committee Approval obtained for this study? No
• Was informed consent obtained from the subjects involved in the study? No
• For any images presented appropriate consent has been obtained from the subjects. No

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