Tuesday, 16 December 2014

A Guide to Periodontology


Periodontitis is becoming ever more evident in the media recently, with lots of press linking a poor periodontal condition to cardiovascular disease, diabetes and even erectile dysfunction!

As patients are living longer, they expect their teeth to last a lifetime and there is greater awareness which both contribute to the rise in litigation against dentists who fail to diagnose periodontal disease. 

Here I will discuss the importance of spotting gum disease and how to manage the condition. 

How is Periodontitis classified?


Since the British Society of Periodontology (BSP) changed it classification of this disease in 1999, periodontitis is classified into 8 different types:
  1. Gingivitis
  2. Necrotising Ulcerative Gingivitis/Periodontitis
  3. Chronic Periodontitis
  4. Aggressive Periodontitis
  5. Periodontal abscesses
  6. Perio-endo lesions
  7. Gingival hyperplasia
  8. Periodontitis as a manifestation of systemic disease
Periodontitis can also be Localised (less than 30% of sites are affected) or Generalised and also mild, moderate or severe. 
Mild: 1-2mm clinical attachment loss
Moderate: 3-5mm clinical attachment loss
Severe:  more than 5mm clinical attachment loss (CAL)

See more about the classification of periodontal disease here 


What cases can I treat in practice? 


The BSP released some guidelines to help GDPs decide which cases can be treated in general practice and which cases they may consider a referral appropriate. They follow in terms of complexity:

1. BPE scores between 1 and 3 - Treat in General Practice

2. BPE scores of 4 - Treat in General Practice or consider a referral for periodontal surgery

3. Surgical cases which involve implants, cases which require tissue augmentation or crown lengthening, patients younger than 35, patients who smoke more than 10 cigarettes a day, complex medical histories, complicated root morphologies or more than 2mm of CAL in 1 year - Refer to specialist



A BPE score of 4 - this could warrant a referral to Specialist services


Risk Factors


The 2 main risk factors for periodontitis are PLAQUE and SMOKING.

Whilst in some forms of periodontitis (e.g. aggressive), plaque control doesn't correlate with the severity of the periodontal disease, poor oral hygiene is the major factor for the breakdown of the periodontal tissues.

Smokers are 2.8 more times at risk to periodontal disease than non-smokers. This is because:
  • There is decreased blood flow to the tissues
  • Smoking impairs white blood cell function
  • There is impaired wound healing
  • There is an increased production of inflammatory mediators which leads to periodontal breakdown
Studies have shown that there is 1mm less probing depth reduction in smokers following non-surgical management of periodontal disease compared to non-smokers. 

Whilst poorly controlled diabetes can aggravate the periodontium, if a patient's diabetes is well controlled then there is no increased risk of periodontal destruction than non-diabetics. 


When should I start performing a Basic Periodontal Examination (BPE)?

Look at a child's incisors and 1st molars, as these are the teeth that can be affected earlier on if life if a patient suffers from aggressive periodontitis.
Examine one tooth in each quadrant.
Aged 7-11: Use codes 0-2
Aged 12+: Use codes 0, 1, 2, 3, 4, *


How much reduction in pocket depths can I expect following successful treatment?


Whilst the main reduction in pocket depths is due to the resolution in inflammation i.e. recession, there is some reattachment of long junctional epithelium at the base of the pocket. 

In pockets 1-3mm, there is on average 0.03mm reduction in probing depths.

In pockets 4-6mm, there is an average of 1.29mm reduction.

And in pockets greater than 6mm, there is an average 2.16mm reduction.

Studies have also shown that you can measure up to a 0.8mm reduction in probing depths from improvement in oral hygiene ALONE.

Options for non-responsive cases.


  1. Another round of non-surgical management (NSM), if there is a potential to heal further and residual subgingival calculus is felt or seen.
  2. Accept and maintain
  3. Extraction of teeth of poor prognosis and assess restorative and aesthetic solutions
  4. Referral for specialist treatment, either privately or to a hospital.
Cases which have furcation involvement may be difficult to treat in practice and there are several options to manage these areas:
  • Scaling and root instrumentation alone
  • Furcation plasty
  • Root resection
  • Tunnel preparation
  • Guided Tissue Regeneration (GTR) - only suitable in some cases
  • Extraction

Should I use Antibiotics?


In general practice, it's not very often that antibiotics are prescribed in the management of periodontitis (unless a patient has a periodontal abscess).
The disadvantages such as the spread of resistance, the disturbance of ecological equilibrium and general side effects of antibiotics often outweigh any beneficial effects.

Systemic antibiotics are widely distributed throughout the mouth, but also throughout the whole body so their effects can be diluted.
Studies have shown that there was a significant difference in the improvement of CAL when using metronidazole in combination with NSM and there was better results in aggressive and refractory types and in deep pockets.
There is no guidance on what dosage to use or for how long, but in these severe cases, the action of metronidazole is on Actinobacillus actinomycetemcomitans.

Localised antibiotics such as doxycycline polymer, minocycline gel or tetracycline fibres act on the sites you place them at, but they need to be able to reach the base of the pocket and be maintained there which can be a problem due to the constant flushing effect of Gingival Crevicular Fluid (GCF).

Periostat can also be prescribed. This is 20mg of doxycycline taken twice a day for 3-9 months. This sub-microbial dose of antibiotics suppresses collagenases and matrix metalloproteinases (MMPs) so there is less periodontal breakdown. 


Guided Tissue Regeneration (GTR)


The basis behind this treatment is to prevent the downgrowth and reattachment of the long junctional epithelium as only periodontal cells e.g. fibroblasts, cementoblasts are able to regenerate the periodontium and these cells are much slower than long junctional epithlial cells to colonise the base of the pocket.

GTR is not effective in treating all cases. It works best in angular 3-walled defects or class II furcations and the narrower the defect, the more predictable the outcome. 

Bone grafts are used e.g. BioOss as well as barrier membranes which cover the graft material e.g. BioGuide. There is some evidence to support just placing the barrier membrane without the bone graft eliminates the recolonisation of long junctional epithelial cells - but it's prudent to place bond grafts in large defects as it preserves the space so you can place the membrane.


This was yet another informative study day - and two weeks on the trot we got to practice surgical procedures on pig's heads! (mind the pun) Thanks to Neesha Patel and her team for a great study day.

To see the effect of an aging population has on the treatment of periodontal disease, please see my post about a talk by the renowned Prof Francis Hughes here.


Please leave any questions or thoughts in the comments below! I'd love to hear other people's views about when they decide to refer periodontal patients to secondary care!

Why not take a look at my other Clinical Guide posts?



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