Chronic infection and inflammation produced by bacterial enzymes and endotoxins that causes deterioration of the periodontium (gingiva, periodontal ligament, cementum, alveolar bone).

 

 

Many scientific studies show that prevalence and severity of periodontal disease is higher in smokers as compared to non-smokers.

 

 

·             Bleeding on probing, redness and exudation – due to peripheral vasoconstriction and/or the inhibition of the immune system caused by tobacco

·             Clinical attachment loss – due to progressive inflammatory process

·             Periodontal pocket depth

·             Recession

·             Alveolar bone loss – due to bone resorption caused by increased osteoclastic activity

·             Number of diseased sites

·             Healing following the periodontal treatment, both surgical and non-surgical – due to impeded function of the cells involved in repair and regeneration.

 

Tobacco is one of the most influential contributing factos in the development and progression of periodontal disease. The toxic substances in tobacco disrupt the harmonic relationship that exists between the host and the oral environment.

 

1. Microflora:

    Although still inconclusive, there is an  evidence that Actinobacillus  Actinomycetemcomitans and Bacteroides forsythus are higher in numbers and

    harder to eradicate after periodontal treatment in smokers.

 

2. Neutrophils:

• Impaired phagocytic activity due to the inhibited production of oxygen radicals, and direct absorption of oxygen radicals by nicotineà decreased antimicrobial  capability
• Impaired chemotaxis due to alteration of  the expression of adhesion molecules

 

3. Immunoglobulins

•   Decreased salivary IgA, suggesting the immunosupressive effect of the toxic substances in tobacco
•   Decrease in serum IgG, suggesting a decrease in antibody response to periodontal pathogens

 

4. Fibroblasts

   -Impaired regenerative capabilities due to inhibited production of collagen, adhesive glycoprotein fibronectin, and alkaline phosphatase

   -increased destructive capabilities due to increased collagenase production --> increased degradation of collagen.

   -disruption of normal cell orientation and vacuolization of the cytoplasm.

 

 

Assessment

·           Identify smoking status as part of health history documentation

·           Perform a comprehensive periodontal exam

 

Diagnosis

·           Consider a possibility of active periodontal disease in a smoker without the signs of active inflammation.

 

Planning

·           Provide smoking cessation counseling and support

·           Consider adjunctive treatment: chemotherapy

·           Consider the possibility of having shorter SPT intervals

 

Implementation

·           Educate about the effects of smoking on the periodontium

·           Emphasize the importance of meticulous self-hygiene

 

Evaluation

·           Evaluate the changes in progression of periodontal disease

·           Follow up with tobacco cessation

·           Consider the possibility of referral to a specialist

·           Refer to tobacco cessation programs in a community