More and more evidence points to smoking as a major risk factor for gum disease (periodontitis). Smoking can affect the prevalence, extent, and severity of the disease. Smoking can also influence the clinical outcome of nonsurgical and surgical periodontal therapy as well as the long-term success of dental implants.
The increased prevalence and severity of periodontal destruction associated with smoking suggests that the host-bacterial interactions normally seen in chronic periodontitis are altered, resulting in more aggressive periodontal breakdown. Although the exact mechanisms are not known, it appears that the host response to bacterial plaque and the ability of the wound healing response in the host are significantly affected. It is believed that much of the impairment is centered around vascularity and the ability to provide nutrients and oxygen to the affected tissue. Studies have shown that current smokers do not respond as well to periodontal therapy as former smokers or non smokers.
The detrimental effects of smoking on treatment outcomes appears to be long-lasting and independent of the frequency of maintenance therapy. Studies show that smokers tend to have deeper periodontal pockets (the deeper the pocket, the worse the disease) than non-smokers and do not respond as well to periodontal therapy as compared to non-smokers.