smoking and its effect on periodontal health
Smoking is the major risk factor for periodontitis and it has an adverse effect on any surgical and nonsurgical therapy. Tobacco smoke contains thousands of noxious chemicals and it has a solid phase and gaseous phase. The gaseous phase contains carbon monoxide, ammonia, formaldehyde, hydrogen cyanide, and many noxious and irritant compound and includes 60 known carcinogens such as benzopyrene and dimethylnitrosamine. The solid phase has “tar” which is inhaled In condensed the sticky brown substances which stain the fingers and yellow and brown.
I) Heavy Smokers - Smokes > 20 cigarettes per day
II) Light Smokers - Smokes < 19 cigarettes per day
GINGIVITIS
The development of inflammation in response to plaque accumulation is reduced in smokers compared to nonsmokers. Smokers usually present with less gingival inflammation than non-smokers.
PERIODONTITIS
Smoking has the highest risk factor for increasing the severity of periodontal destruction. Subjects who smoke 30 or more cigarettes per day were almost 6 times more likely to have periodontitis, Smokers are pronounced to have periodontitis 4 times more than nonsmokers. Its effects include,
1. Increased rate of periodontal destruction.
2. Increased tooth loss.
3. Increased prevalence with an increase in the number of cigarettes smoked per day.
4. Decrease and severity of smoking cessation gums(gingiva).
Due to the effect of smoking, the gingiva becomes dark and pigmented called "Smoker's Melanosis" Another condition called "Smoker’s palate" or "Nicotine stomatitis" is seen in the palate due to the heat of tobacco and its irritation on the mucous membrane.
Effects of smoking on the etiology and pathogenesis of periodontal disease
Microbiology
It does not affect the rate of plaque accumulation. Increased colonization of shallow periodontal pocket by periodontal pathogen. Increased level of the periodontal pathogen in deep periodontal pockets
Immune inflammatory response. Altered neutrophil chemotaxis, phagocytosis, oxidative burst. Increased tumor necrosis factor-alpha and prostaglandin E in gingival crevicular fluid. Increased neutrophil collagenase and elastase in gingival crevicular fluid. Increased production of prostaglandin E by monocytes in response to lipopolysaccharides.
Physiological response
1. Increased gingival blood loss with increased inflammation.
2. Decreased gingival crevicular fluid flow and bleeding on probing with increased inflammation.
3. Decreased subgingival temperature.
4. Increased time needed to recover from local anesthesia.
Effects of smoking on response to periodontal therapy
Nonsurgical therapy
Studies indicate that current smokers do not respond as well to periodontal therapy as nonsmokers or former smokers do. Pocket depth reduction is more effective in nonsmokers than in smokers after nonsurgical periodontal therapy including oral hygiene scaling and root and root surface debridement. Gain in clinical attachment loss in non-surgical therapy is more in the nonsmoker. when a higher level of plaque control is achieved in nonsurgical 4 to 6 mm of pocket between nonsmoker and smoker become clinically less significant. It can be concluded that smokers do not respond as well to nonsurgical therapy as a nonsmoker. So, patients should be given proper counseling about smoking cessation and its importance in periodontal therapy.
Surgical therapy and implants
Smoking has adverse effects on guided tissue regeneration and infrabony defects by a bone graft. It has been observed the use of bone grafts in nonsmokers has less reduction in pocket depth than in smokers. Open flap surgery without regeneration and grafting procedures is the most common surgical procedure that is to be carried out for accessing the bone and root surfaces. By 6 months after the procedure smoker shows less reduction in a deep pocket and clinical attachment loss than the patient who has undergone an implant smoking increases the risk of implant, and the risk of implant failure is doubled in smokers than in nonsmokers. Smoking may also increase the cause of periimplantitis (inflammatory process affects the surrounding tissue of the implant and result in the loss of supporting bone). It is necessary for all patients who have to be undergone implant therapy should be informed about the benefits of smoking cessation and the risk of periimplantitis and implant failure.
Maintenance therapy
After different modalities of therapy ( scaling and root flap surgery, osseous surgery maintenance therapy was to be performed every 3 months for 7 years. The duration of maintenance therapy should be extended for a smoker than for a nonsmoker. smoking has detrimental effects on patients implant patients should have strict maintenance care to prevent periimplantitis. Although the maintenance therapy is performed regularly it is important to quit smoking for recurrent risk and to achieve positive treatment outcomes.
Smoking cessation has a positive outcome for periodontal when the subject received nonsurgical or surgical periodontal therapy and along with smoking cessation counseling for 12 months and quit smoking successfully , he /she had the best response to the periodontal treatment.
The benefits of smoking on periodontium are,
1. Less pathogenic microbiota in oral flora.
2. Improvement in gingival microcirculation.
3. The increased immune-inflammatory reaction.
4. Smoking cessation plays a vital role in periodontal therapy for patients who smoke.
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