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Why is smoke so harmful for dental implants?

 

The link between smoke and implant failures


Data show that smoke is the first cause, after aging, that leads to periimplant bone loss.

416 subjects, undergoing caries treatment at the Washington University, were examined through X-rays to assess bone loss in relation to aging. 73.9% of young people and 100% of the aged ones showing bone loss were smokers. Data show that smoke is the first cause, after aging, that leads to periimplant bone loss.

R.E. Persson, L.G.Hollender, G.R. Persson. Assessment of alveolar bone levels from intraoral radiographs. J.Clin.Periodontol. 1998; 25:647-654


Women who smoke one pack of cigarettes each day throughout adulthood will, by the time of menopause, have an average deficit of 5 to 10 percent in bone density, which is sufficient to increase the risk of fracture.

Hopper JL, Seeman E. The bone density of female twins discordant for tobacco use. N Engl J Med. 1994 Feb 10;330(6):387-92.


Is there any correlation between the habit of smoking and failures in Implantology?


Heavy smokers, or people having been exposed to smoke for years, show greater bone loss and periodontal probing depth than light smokers, or people having been exposed to smoke for a shorter time.

J. Bergstrom: “Dose-dependent periodontal disease response to tobacco smoking” Europerio 2 Florence-Italy May 15-17, 1997

The aim of the present study was to examine the dental status and smoking habits in randomized samples of 35-, 50-, 65-, and 75-year-old subjects In 75-year-olds, 41% of the smokers were edentulous compared to 35% of non-smokers. The difference in number of missing teeth between smokers and non-smokers was 0.6 (p=0.15), 1.5 (p=0.013), 3.5 (p=0.0007) and 5.8 (p=0.005) in the 4 age groups. Smokers had the largest mean probing attachment loss in all age groups. The number of intact tooth surfaces was fewer in 35-, 50-, and 75-year-old smokers than in non-smokers. The number of missing surfaces (MS) was higher in 50-, 65-, and 75-year-old smokers than in non-smokers. In addition, 35-year-old smokers exhibited a significantly larger number of decayed and filled tooth surfaces (DFS) than non-smokers. It was concluded that smoking is a significant risk indicator for tooth loss, probing attachment loss and dental caries.

Axelsson P, Paulander J, Lindhe J. Relationship between smoking and dental status in 35-, 50-, 65-, and 75-year-old individuals. J Clin Periodontol. 1998 Apr;25(4):297-305.


At present, the main factors leading to implant failures are scarce bone density and smoking.

Bain CA. Smoking and implant failure--benefits of a smoking cessation protocol. Int J Oral Maxillofac Implants. 1996 Nov-Dec;11(6):756-9.


Even if bone quality was similar between the two groups, we observed a 9% failure rate in smokers vs. 1% in non-smokers. Smoking, therefore, is a significant (even if not unique) factor causing implant failure before functional loading.

De Bruyn H, Collaert B. The effect of smoking on early implant failure.Clin Oral Implants Res. 1994 Dec;5(4):260-4.

Why has smoke such a negative effect on implant success? We hypothesize that smoking prompts the development of a less dense bone structure.

Women who smoke one pack of cigarettes each day throughout adulthood will, by the time of menopause, have an average deficit of 5 to 10 percent greater than non-smoker ones in bone density  .

Hopper JL, Seeman E. The bone density of female twins discordant for tobacco use. N Engl J Med. 1994 Feb 10;330(6):387-92.


We assessed more than 1,200 dental implants. Type IV (i.e. low density) bone has been observed in a 2:1 ratio between smokers and non-smokers. Bain CA ,May PK:”The influence of smoking on bone…” Int. J. Oral Maxillofacial Impl. 1993; 9:123-128

Vertical bone loss was assessed from intraoral radiographsin  416 subjects seeking dental care at the University of Washington.  73.9% of the younger and 100% of the older subjects with severe alveolar bone loss were smokers. Data show smoking is the first cause of alveolar bone loss, followed by aging.

Persson RE, Hollender LG, Persson GR. Assessment of alveolar bone levels from intraoral radiographs in subjects between ages 15 and 94 years seeking dental care. J Clin Periodontol. 1998 Aug;25(8):647-54.


412 patients, bearing 1379 dental implants were observe during a 5-year follow up. Implant failure rate was 4.92% in smokers vs. 15.06% in non-smokers. Type IV bone quality was observed in 17.6% of non-smokers vs. 37.9% of smokers.

Bain CA ,May PK:”The influence of smoking on bone…” Int. J. Oral Maxillofacial Impl. 1993; 9:123-128

We had formulated an hypothesis: that smoke leads to develop a less dense bone structure. On the basis of international literature this hypothesis corresponds to the truth. A second hypothesis is that smoking exerts a negative effect on the immune system. Nicotine alters fibroblasts adhesion on radicular surfaces and an alteration of the antibody status against P. intermedia and F. nucleatum, lowering serum level of IgGs directed against these microorganisms.

Sforza NM.  “Smoke habit and periodontal disorders” Dental Cadmos 1996; 12:46-67

We studied how periodontal ligament fibroblast adhesion is influenced by the presence of nicotine. Inhibitions spans from 5% at the lowest nicotine concentration (50 mg/ml) to 90% at the highest (250 mg/ml), and was more evident at the second day of exposition. Poulon GG, Geinoz A, Cimasoni G. ”Nicotine effects of periodontal ligament fibroblasts in vitro”.  Europerio 2 Florence-Italy 15-17 May 97

Cigarette smoke showed to interfere with polymorphonuclear cells and with their phagocytic activity. Tobacco’s negative effects, linked to the persistence of toxic residuals in the mouth, lasts from 1 to 3 years.

Kenney EB, Kraal JH, Saxe SR, Jones J. The effect of cigarette smoke on human oral polymorphonuclear leukocytes. J Periodontal Res. 1977 Jul;12(4):227-34.

This study examined the effect of nicotine on periodontal ligament fibroblasts as far as their proliferation, adhesion, alkaline phosphatase activity and chemotaxis were concerned. Cell proliferation was inhibited at a 100 ng/ml dose. The same dose inhibits adhesion and such effect is even more evident after 6 hours. The phosphatase production is severely impaired. Chemotaxis is reduced by 15% at a nicotine concentration equal to 5 ng/ml. Reduction reaches 90%  if concentration is  50 ng/ml.

Giannopoulou C, Geinoz A, Cimasoni G. Effects of nicotine on periodontal ligament fibroblasts in vitro. J Clin Periodontol. 1999 Jan;26(1):49-55. We had formulated the hypothesis that smoking is harmful to the immune system, and we can conclude – on the basis of the literature cited – that such hypothesis is true.

We hypothesize, also, that smoking modifies blood circulation and microcirculation, resulting in bone and soft tissue damage.

Nicotine exerts a vasoconstrictor effect reducing blood supply to the healing region, and could provoke thrombotic-like microvascular occlusions leading to partially ischemic areas. Gonzales YM. ”Smoking as a risk factor” Dental Cadmos 1997; 5:56-60


It looks reasonable hypothesizing that reduced bone vascularization is the main mechanism underlying implant failure in smokers, since blood flux already increases after one week smoking is suspended.

Bain CA. Smoking and implant failure--benefits of a smoking cessation protocol. Int J Oral Maxillofac Implants. 1996 Nov-Dec;11(6):756-9.

Smokers show blood flux speed modifications in their peripheral districts. Such variations may be induced both by nicotine-induced hormonal changes (catecholamine) and by direct active effects on vessels (vasopressin-neurophysin) and also, finally, by a direct in toto action of smoke on oral mucosa capillaries. Cavagna S, Leghissa GC: “Correlation between periodontal pathology, therapy and implants…” Implantologia Orale 2000;1:38-42

A flux ultrasonic measuring doppler device has been used to check hematic speed in two groups of male volunteers. It was observed that smoking a single cigarette reduces blood speed, at peripheral level, by a 42%.

“Thermogram of arms before and after a cigarette. Nicotine reduces blood vessels  lumen, diminishes blood flux and right arms are colder”. Focus 05/2012

This work has highlighted how subgingival temperature increases when periodontal pockets deepen. Therefore, there’s a differential in temperature between the subgingival and the sublingual compartment.

L.Chamam:”Effect of smoking…” J.Am. Dental Ass. 1974; 10:1327-28

Smokers show an increase of temperature in, at a probing depth of 2 to 5 mm, significantly smaller than  non-smokers. Trikilis N, Rawlinson A, Walsh TF. Periodontal probing depth and subgingival temperature in smokers and non-smokers. J Clin Periodontol. 1999 Jan;26(1):38-43.

Also the hypothesis that smoking is harmful to bone and soft tissues impairing circulation was shown  – on the basis of the literature cited – to be true.

Branemark suggests a smoking suspension protocol to be activated 1 week before and prolonged 8 weeks after implant positioning surgery.

223 Branemark implants were positioned in 78 patients, divided into 3 groups: non-smokers, smokers adhering to the suspension protocol, smokers continuing to smoke. Implant failures was observed in 5.68 % of non-smoking patients, 11.76%  of smokers having suspended smoking, 38.46% of patients still smoking.

Bain CA. Smoking and implant failure--benefits of a smoking cessation protocol. Int J Oral Maxillofac Implants. 1996 Nov-Dec;11(6):756-9.