1. Our current understanding of the aetiology of periodontitis is that disease results from an upset in the balance between the biofilm and host response. Bacteria are required for the initiation of periodontitis but the host response and associated risk factors determine susceptibility and progression. 80% of the damage in periodontitis is likely to be down to an inappropriate host response. Inflammation and the immune system are components of the host response. An inappropriate response can be an under-performing or (more usually) an over-vigorous host response. Therefore, periodontitis may be seen as an autoimmune condition with an inflammatory basis rather than a typical ‘infection’.
2. The host response can be modified by a number of risk factors e.g. genetics, smoking, stress, diabetes, nutrition, obesity and perhaps by lifestyle (lack of exercise, sleep deprivation, depression).
3. According to the Adult Dental Health Survey (2009), the prevalence of severe (6 mm + pockets) has increased. This is not due to poor oral hygiene as we are cleaning our teeth better than in the past. This may be associated with other risk factors e.g. an increase in diabetes and changes in lifestyle.
4. Definitions: A risk factor is a characteristic of a person or their environment which, when present, directly result in an increased likelihood of that person getting the disease, and when absent directly results in a decreased likelihood (Beck et al 1995). Risk factors may have a causal relationship and examples include genetics, smoking, stress and systemic disease. A risk marker/predictor is not causally related but their presence is more a consequence of the disease being present e.g. bleeding on probing, mobility, recession and suppuration.
5. Risk factors for periodontitis can be divided into local and systemic factors. Local would include plaque retentive factors such as root grooves, restoration margins, impacted teeth, dental appliances etc. Systemic risk factors would include genetics, smoking, stress, diabetes, and nutrition. Risks can be non-modifiable (biofilm, genetics, sex) or modifiable (smoking, diabetes, nutrition). It is important to complete a risk assessment when you first see your patient. Patients should be informed of any risks that are picked up and you should also document these discussions in the patient’s notes.
6. Biofilm – Probably better thought of as the primary aetiological factor rather than a risk factor. Optimal oral hygiene is crucial to controlling periodontitis (Lindhe & Nyman 1975, Pihlstrom et al 1983, Renvert et al 1990). Poor supragingival plaque control following therapy results in continued attachment loss (Nyman et al 1975, Axelsson & Lindhe 1981, Westfelt et al 1983). The most important factor in the prevention and treatment of periodontitis is the individual’s standard of daily self-performed oral hygiene (Stenman 2012). Educate, motivate and demonstrate oral hygiene techniques. An interspace brush can be very helpful in reaching pockets (Page & Rams 2013).
7. Genetics – Hypo-responsive (defective PMNs or phagocytosis) or hyper-responsive (enhanced cytokine production). Both can result in increase susceptibility and tissue damage. Monozygous twin studies indicate that at least 50% of periodontitis is due to genetics (Michaelowicz 1991). There have been a number of candidate genes identified e.g. IL-1, but currently available tests are limited. Take a through family history and consider monitoring other family members.
8. Smoking – The most important modifiable environmental risk factor. As many as 42% of periodontitis cases may be attributed to smoking (NHANES 2000). 22% of patients in the UK are smokers (ADHS 2009) – this has decreased over the last few years. 70% of patients would like to quit (HBRC 2007) but only 9% of patients in the UK have been given cessation advice by their dentist in the last 2 years (ADHS 2009). Smoking has a number of direct tissue effects (reduced tissue vascularity, impaired PMN chemotaxis and phagocytosis) and significantly affects the immune response (decreased salivary IgA, IgG and helper T cells). Clinically, smokers will have more and deeper pockets (especially palatally) (Bergstrom 2000), more attachment loss including recession (Haffajee & Socransky 2001), more alveolar bone loss (Bergsrom 2000), more teeth with furcation involvement (Mullally & Linden 1996) and more tooth loss (Krall et al 1997). Heavy smokers (10 + cigarettes/day) have a 3 times higher likelihood of losing their teeth compared to non-smokers (Dietrich et al 1990) – this is a good figure to quote to your patients. The severity of periodontitis is related to the duration of tobacco use, smoking status and daily intake (AAP 1996). It is important to encourage patients to quit rather than cut down. When considering treatment, smokers will benefit from periodontal therapy but clinical improvement will be less than those for non-smokers.
9. Diabetes – The prevalence of diabetes in the UK is 5.5% (2011) but there are equal numbers of undiagnosed diabetics. The WHO estimates a global burden of 10% of adults by 2030. There is a bi-directional relationship between uncontrolled diabetes (glycaemic control) and periodontitis. Look out for high-risk groups and consider referral for suspected diabetics. If your patient is diabetic then ensure it is well controlled.
   
10. Nutrition – Micronutrients can be agonists (pro-inflammatory e.g. refined carbohydrates and saturated fats) or antagonists (anti-inflammatory e.g. vitamins and polyphenols) of inflammation (Chapple et al 2009). Refined carbohydrate intake drives systemic or ‘meal-induced’ inflammation using the Krebs cycle that leads to the production of free radicals and ‘oxidative stress’. Oxidative stress is a key pathological event underpinning periodontal tissue destruction (Chapple et al 2012). In the study by Tomofuji et al 2011, overweight students frequently consuming fatty foods had an increased risk (odds ratio of 2.3) of periodontitis. It may be a good idea to ask your patients to complete a 3-day diet sheet, which can later be analysed to highlight the pro- and anti-inflammatory food groups.
11. Stress – Stress causes altered habits including reduced oral hygiene but also has an impact on immune function. The coping mechanisms associated with stress are more important than the stress itself (Wimmer et al 2002).
12. Sex – There seems to be a 9% difference between males and females, with men appearing to have a greater risk than women (Shiau & Reynolds 2010). These sex differences are likely to be associated with behaviour rather than biology. Furthermore, there appears to be a lack of relevance of hormonal change to periodontal attachment levels i.e. patients may suffer from pregnancy gingivitis but this is not translated to pregnancy periodontitis.
13. Drugs – Some drugs can cause drug-induced gingival overgrowth e.g. anticonvulsants (phenytoin), immunosupressives (cyclosporine) and antihypertensives (calcium channel blockers – nifedipine, amlodipine). It may be worth writing to the GP to explore whether a drug change is a realistic option. Otherwise these cases are usually managed non-surgically. In severe cases, surgery may be considered.
14. Periodontal management must always involve a risk assessment. Periodontitis is a multi-factorial disease and we need to help the patient to control modifiable risk factors. Failure to follow advice about controlling modifiable risk factors should be documented as non-compliance.
15. There are now tools available to help assess the patient’s risk of periodontitis (e.g. PreViser) as well as establish maintenance recall intervals based on risk factors (Lang & Tonetti 2003).

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Periodontology