Although the role of oral health in systemic disease has been recognised for over a millennium, the bacteria of the complex microbial biofilm that forms dental plaque and which are the cause of periodontal disease and gingivitis, have only recently been implicated in specific conditions such as coronary heart disease and stroke, or higher risk of preterm low birth-weight babies, and as a risk compounding factor in those with chronic disease such as diabetes, respiratory disorders and osteoporosis.
The aetiological and pathological mechanisms behind these associations remain unknown, although hypotheses such as common susceptibility, systemic inflammation with increased circulating cytokines and mediators, direct infection and cross-reactivity or molecular mimicry between bacterial antigens and self-antigens have all been suggested.
The implication, that control of oral disease is essential in the prevention and risk reduction of systemic conditions, is increasingly recognised and may prove an essential tool in the management of many chronic diseases. Also, many of these associations are two-way, that is, the disease itself is affected by periodontal disease and can in turn affect the oral environment, bacterial populations and oral health.However, further research is core to
the better management of diseases associated with oral disease.
Cardiovascular disease and stroke
Several studies have shown that periodontal disease is associated with the development of heart disease. Also, periodontal disease has been demonstrated to exacerbate existing heart conditions which is why, for example, patients at risk of infective endocarditis, such as those with known valvular disease, are given antibiotics prior to dental procedures.
An inflammatory effect is likely to be responsible, but current studies have yet to demonstrate the exact pathophysiology behind the association – whether the cause is direct bacterial infection of the vascular wall or through the stimulation of a pro-inflammatory state by periodontitis (or possibly both, simultaneously). The distinction is vital for developing treatment strategies for periodontal disease, as some therapies, such as scaling and root planing, may promote the heamatogenous seeding of bacteria, increasing the risk if direct infection is the cause.
Future studies around evaluating effectiveness in reducing cardiovascular events through the prevention of periodontal disease will require the incorporation of detailed antibiotic and anti-inflammatory strategies. Other studies are needed to advance the evidence gained so far which also shows periodontal disease as a risk factor for stroke, including studies which show that people diagnosed with acute cerebrovascular ischemia are more likely to have an oral infection when compared to control groups.
Diabetes
People with diabetes are more likely to have oral infections, bacterial and fungal, and periodontal disease, than people without diabetes, as a result of their susceptibility to local and systemic infection associated with poor glucose control. However, periodontal disease can then itself adversely affect blood glucose control, further influencing the systemic inflammatory changes associated with persistent hyperglycaemia.
The current hypothesis supporting the concept that chronic inflammation caused by periodontal infection contributes to the pathogenesis of type 2 diabetes needs further clarification. Within this, a logical framework with greater clarity of the mechanism behind periodontal infection and cardiovascular disease is needed, leading to a hypothesis unifying both these inflammatory diseases and offering a unique opportunity for reducing complications associated with both.
Osteoporosis
The link between osteoporosis and bone loss in the jaw is well established, with osteoporosis leading to tooth loss as a result of poor structural support from decreased bone density. In the relationship between periodontal disease and osteoporosis, detailed knowledge of the molecular mechanisms involved in RANKL-RANK activation and downstream signalling could generate new pharmacological principles for the inhibition of excessive bone resorption in pathological conditions.Furthermore, additional longitudinal studies may be necessary in exploring the use of osteocalcin, parathyroid hormone, and calcitonin as diagnostic indicators of periodontal disease activity. In addition to these research topics, further studies of the mechanism of nitric oxide effects on alveolar bone are needed, in association with an understanding of the indications for isosorbide in treating periodontal infection.
Respiratory disorders
There is some research to suggest that higher levels of oral bacteria, associated with periodontal disease, may lead to aspiration of bacteria into the respiratory tract and a higher risk of pneumonia and other respiratory infections.
Cancer
Periodontal disease has been suggested as a causative factor in certain types of cancer. In a study of over 48,000 men in 2008 there was a small but significant increase in overall cancer risk which persisted in never-smokers. The associations recorded for lung cancer were probably because of residual confounding by smoking, but the increased risks noted for haematological, kidney, and pancreatic cancers suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk.
Low birth weight
The mechanisms by which maternal periodontal disease may reduce birth weight are not clear and may be causal or simply associative, although there is evidence that this association has a biologically feasible basis. Periodontitis is a modifiable risk factor for several serious systemic conditions, including pregnancy complications and it may be of importance in obstetric care.
What is clear is that more research is needed, both around causative mechanisms and management strategies. In the meantime, simple health advice, not just from dentists and hygienists but also from primary care teams, around brushing, flossing and limiting other risk factors such as smoking, will help to decrease periodontal pockets , reducing periodontal bacterial populations and hence the likelihood of the associated systemic disease.
References available on request.