September 19, 2014

Why it’s important:

  • Litigation is on the increase and patient’s expectations have increased. There has been a 32% increase in the number of claims made against dentists. The DDU paid out £2.8 million in compensation during the year of 2012.
  • Lack of communication can turn patients into angry ones in a matter of seconds – good communication is essential!
  • A study from Norway found that dentists spend 3.1 mins/year per pt on periodontal treatment. 90% of patients that were referred to the periodontal department in Bergen did not know they suffered from periodontal disease.
  • Good note keeping is also crucial – keep detailed notes! A BPE must form part of this as a minimum and needs to be taken at least once a year.

Aetiology and risk factors:

  • Our concept of periodontal disease has changed over time. The early concept of a linear model depicted the principal etiologic role of bacteria and risk factors included OH and age. Loe’s study in Sri Lanka in 1986 found that individuals have a range of susceptibilities. In the 1980’s a model was created that emphasised the central role of the host immune-inflammatory response. The current model includes specific innate, acquired and environmental factors.
  • The host is responding to the challenge to protect the body but at the same time this causes by-stander damage.
  • The development and progression of periodontitis depends on specific inherited, behavioural and environmental risk factors.
  • Risk factors may be modifiable (environmental/behavioural) or non-modifiable (intrinsic to individual).
  • Risk factors – smoking, diabetes, stress, systemic disease, nutrition, tooth related. Risk determinants – genetics, socioeconomic status, gender, age?
  • Smoking – strong risk factor attributed to current and former smoking, severity is directly related to number of cigarettes a day and number of years. Clinically, smokers have reduced gingival bleeding and inflammation but greater pocketing. Odds ratio – 6.8. If a patient stops smoking an used to smoke half a pack a day, they can save themselves £28653 over 20 years (assumed pack £7.85).
  • Diabetes – type 2 is on the increase. Factors contributing include the degree of control and age of onset. Diabetes impairs the host response and healing capacity.
  • Stress – such as negative life events have an impact on the function of the immune system.
  • Drugs – anticonvulsants, immunosuppressants, and calcium channel blocking drugs induce gingival overgrowth that classically begins in interdental papillae region. This makes plaque control more difficult and therefore you create a viscous cycle.
  • Systemic disease – HIV infection (necrotising gingivitis/periodontitis), blood dyscrasias, scurvy and pregnancy.
  • Nutrition – severe vitamin C or D deficiency is a risk factor.
  • Genetics – 50% of susceptibility to periodontitis may be due to host factors. Major role in determining susceptibility. Important to consider genetic polymorphisms e.g. IL-1 polymorphism.
  • Socioeconomic status – tend to be heavier smokers with poor plaque control.
  • Gender – periodontitis is higher in males.
  • Age – age is not a risk factor per se.
  • Tooth related factors – plaque retention areas, occlusal discrepancies, anatomical (pearls, grooves, furcations), tooth position (crowding, tipping, migration, occlusal forces) and violation of biologic width.

Methods of treatment:

  • The goal of preserving the natural dentition and foundation in decision making has been altered. As the modern implants offers excellent choice, the value of natural teeth reduced.
  • Oral hygiene – when you brush your teeth you only clean 60% of the surfaces of the teeth. It’s important to maximise the results of interdental cleaning.
  • Oral hygiene instructions: Be specific, make it easy, give snippets of information, help the patient build it into their routine and decide on reminders to jog memory if required.
  • Following on with root surface debridement, possible chemical adjuncts and possibly surgery.


  • Peri-implant mucositis is reversible and can be compared to gingivitis. Peri-implant disease is irreversible destruction.
  • Survival uses the presence or absence of implant as an end-point – we need to know about bone loss! Survival doesn’t take into account slowly progressing on-going biological problems.
  • Peri-implant disease risk factors –acute infection, large areas of leukoplakia, progressive disease, poor oral hygiene, smoking, previous periodontitis, bacterial factors, biomechanical factors, other co-factors (e.g. cementitis).
  • Ong 2008 systematic review – previous periodontitis patients had a less successful implant survival rate.
  • Diabetes – Ferreira 2006 the only study linking poor metabolic control and increased risk peri-implantitis.
  • Pontoriero et al suggests that the microbiology around implants is more complex than around teeth.
  • Bone loss tends to be crestal – all the way round – need radiographs as baseline to compare.
  • Classification of peri-implantitis – Spiekermann – class 1-4. Stuart Froum – early, moderate and advanced.
  • Initial treamtent – occlusal therapy (check for any excessive forces), antiinfective theapy (remove plaque deposits, titanimum can be used, plastic tips may bend and break), irrigate, local antimicrobials, air abrasion is also useful), systemic antibiotics (supportive therapy), implant surface (preparation). Surgical – resective, regenerative or reosseointegration.
  • Maintenance of implants is essential to ensure good long-term survival.


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