Cardiovascular disease accounts for 29% of deaths worldwide and ranks as the second leading cause of death after infectious and parasitic diseases. Cardiovascular and periodontal diseases are common inflammatory conditions in the human population.

In atherogenesis, inflammation plays a continuous role from endothelial cell expression of adhesion molecules to the development of the fatty streak, established plaque, and finally plaque rupture. Recent research has established that periodontal infection is a probable risk factor for cardiovascular disease, including atherosclerosis, myocardial infarction and stroke. Exposures to infections like periodontal disease have been postulated to perpetuate inflammatory events in atherogenesis. For example, patients with severe periodontitis are almost twice as likely to have a fatal heart attack and three times as likely to have a stroke as patients without periodontal disease, even after adjusting for known cardiovascular risk factors such as blood lipids, cholesterol, body mass, diabetes and smoking.

Recent observational studies and meta-analyses continue to demonstrate a modest but statistically significant increased risk for cardiovascular disease among persons exposed to periodontal disease or infection. Experiments with animal models further indicate that periodontal infection can increase atherosclerosis in the presence or absence of hypercholesterolemia.

While the available pilot data in patients suggest that periodontal interventions can improve surrogate serum biomarkers and vascular responses associated with cardiovascular disease, the effect of these interventions on true outcomes of cardiovascular diseases like myocardial infarction and stroke is presently unknown. Nevertheless, clinicians and patients should be aware of the consistent association between cardiovascular and periodontal diseases along with the potential preventive benefits of periodontal interventions.

Diabetic patients are commonly encountered in the dental office. Proper patient management requires close interaction between the dentist and physician.

Loe in 1993 gave the classic statement - "Periodontitis is the 6th Complication of Diabetes Mellitus." Since then a large body of work exists on the relation between these two diseases.

Recent years have seen an increased appreciation of the role systemic inflammation plays in the patho-physiology of diabetes and its complications. Periodontal diseases are inflammatory in nature; as such, they may alter glycemic control in a similar manner.

Periodontal intervention trials suggest a significant potential metabolic benefit of periodontal therapy in people with diabetes. Several studies of diabetic subjects with periodontitis have shown improvements in glycemic control following scaling and root planing combined with adjunctive systemic doxycycline therapy.

Apart from these links, current research has suggested that periodontitis may predispose to a pre-diabetic state or impaired glucose tolerance in non-diabetic individuals. This relationship needs to be verified with further long-term controlled trials.

The picture of the mother giving birth ''early'' due to a sudden external stressor is well known by the layperson. Worldwide, in all population groups, birth weight is the most important determinant of the chances of a newborn infant to survive, grow and develop healthily. Reducing pre-term birth rates is a formidable, yet critical, challenge to the healthcare community worldwide. Periodontal disease has been studied in association with pregnancy outcomes, including pre-term delivery, low birth weight, pre-eclampsia and miscarriage.

Offenbacher and colleagues were the first to report a link between poor maternal periodontal health and adverse pregnancy outcomes, including pre-term birth, in humans. A recent meta-analysis of two case-control and three prospective cohort studies concluded that maternal periodontal disease was strongly associated with risk for pre-term birth. Another similar analysis reputed this possibility.

Although a variety of evidence suggests some link between the two, there is also agreement that more and larger studies, including intervention studies, are needed to determine if the relationship is causal or coincidental. Currently, there are at least three ongoing randomised clinical studies designed to further explore the nature of this association. At present, however, there is no compelling evidence to indicate that treatment of periodontitis can improve birth outcomes.

Low bone mass (osteopenia) and osteoporosis are systemic skeletal diseases characterized by low bone mass and micro-architectural deterioration with a consequent increase in bone fragility and susceptibility to fracture. Both osteopenia and osteoporosis are grave public health concerns and are widely prevalent in developed countries, particularly among postmenopausal women.

Kribbs was the first to address the relationship between systemic bone mineral density and mandibular density when measured by quantitative analysis on intra-oral radiographs.

The risk factors for osteoporosis include many risk factors associated with advanced periodontal disease. Since both osteoporosis and periodontal diseases are bone resorptive diseases, it has been hypothesized that osteoporosis could be a risk factor for the progression of periodontal disease. Further studies are being conducted to develop protocols for pre-screening our patients for reduced bone mineral density on dental radiographs.

Apart from the above disease states, there exist evidence linking periodontal diseases to systemic conditions, most notably upper respiratory tract infections, renal diseases, cerebro-vascular accidents, etc. A few recent studies have even proposed a link between periodontal disease and increased risk for pancreatic cancer.

Evidence linking periodontal inflammation to many systemic conditions has started to emerge at a rapid rate in recent times. However, lack of standardization in study protocols, presence of various confounding factors, and absence of long-term interventional trials results have been responsible for the confusion in the field of periodontal medicine.

At present, it is still not certain whether the treatments to reduce the oral microbial and inflammatory burden of periodontitis and the clinical end-points that are currently used to manage periodontitis are sufficient or even appropriate to manage these systemic problems. Optimal treatments may be totally different for a high-risk individual. As an example, current periodontal maintenance programs may prevent attachment loss but may not be sufficient to prevent the inflammatory response leading to a heart attack in the susceptible individual.

Dentists must educate patients and their physicians about the importance of periodontal health, with an emphasis on the inflammatory nature of periodontal diseases and the potential systemic effects of periodontal infection. Working with medically compromised patients can be challenging and rewarding when open lines of communication are established and thorough patient education is attained.

It appears highly likely that the new knowledge being gained in the discipline of periodontal medicine will serve as an impetus to further coalesce medicine and dentistry. Dentists will need to assume a larger responsibility for the overall health of patients, and eventually periodontal care may become a medical necessity. Knowledge of relevant systemic conditions needs to be more extensive to enable dentists to interact more meaningfully with their medical colleagues. This will place new educational goals on the profession.