Does smoking cloud implant success?

Nearly 1000 implants were placed in 261 patients: 579 implants were placed in non-smokers and 380 implants in smokers. The smokers were broken down into mild and heavy users. Mild smokers smoked less than 10 cigarettes/day; heavy smokers smoked more than 10 cigarettes/day. These groups were subdivided by whether they smoked less or more than 10 years.

The investigators were not only interested in implant success or failure. They wanted to know if it made a difference to place an implant in an extraction socket the day a tooth is removed, or wait 3 months for the socket to heal before inserting the implant. They also studied how the subjects tolerated flat or high implant cover screws. (Implant cover screws are inserted into the implant head to prevent in-growth of tissue during the healing phase. The intention of the surgeon in this study was to cover the implant and cover screw and not have any portion of the implant exposed to the oral cavity). The results were interesting.

Nine hundred and fifty-nine (959) implants were placed; only 22 failed. Of these, 10 failed in non-smokers and 12 failed in smokers. The failure rate translates to approximately 1% of the non-smokers and 3% of the smokers. All failures in smokers occurred in those smoking 20 or more cigarettes/day and in those who smoked more than 10 years. When it came to the success of immediate (placing the implant the day the tooth was removed) versus delayed placement after healing (waiting 3 months), more failures occurred in delayed healing (78% vs. 22%). More high screws failed in both smokers and non-smokers (64% vs. 36%).

Apart from implant failures, which were few in both groups in this study, more complications were experienced in both smokers and non-smokers when high cover screws were used. The most common complication was perforation of the tissue and exposure of the implant during the healing phase, but these complications did not lead to implant failure.

So what can we glean from this study? For one, a high percentage of implants can successfully be placed in non-smokers as well as in smokers. We also learned that there was more success when implants were immediately placed in extraction sites, and that there were more complications when high cover screws were used. While we discourage all from smoking, the results in this study concur with our own clinical experiences, that implants can successfully be placed in smokers. For this reason, smokers should not be turned away when they require sophisticated dental procedures such as implants and sinus bone grafts. What needs mentioning, however, is that when smokers do have complications such as infections and implant failures, their problems tend to be worse and more difficult to treat than in non-smokers.

*Schwartz-Arad D., Samet, N., Samet, N., and Mamlider A.: Smoking and complications of endosseous dental implants. J Perio 73:153-157, 2002.

When waiting just won't do

We all know that lesions in the mouth deserve our careful attention. White and chronically ulcerated patches on our tongues, inner cheeks, mucosa, and gums need to be investigated. Once discovered, attentive dentists and patients should pursue a variety of options including brush or incisional/excisional biopsies to help determine what the lesions are and what is the best follow-up care. One common lesion - leukoplakia - has always been considered pre-cancerous. While we know that pre-cancerous lesions are just that…pre-cancers…how likely will the prefix "pre" turn into a full-fledged cancer? Is there any predictor when or even if this will occur? Here are some answers.

Researchers* identified 150 patients with oral leukoplakia. These lesions were classified as epithelial dysplasia and then studied to determine if their DNA content (known as ploidy) could be used to predict their future outcome. Each patient had their lesions biopsied annually in order to classify the DNA content. What is important to note is that DNA varies in leukoplakias from normal to abnormal.

Results: Thirty-six (or 24%) of the 150 patients with epithelial dysplasia in this study developed carcinomas, and the occurrence increased relative to the degree of DNA ploidy.

Frequency: One hundred and five (105) of the 150 patients studied had normal diploid lesions. Only 3 of these patients developed carcinomas. Twelve (12) of the twenty (20) patients who had intermediate (tetraploid) lesions developed carcinomas. Abnormal DNA content is found in aneuploid lesions. In this study, 21 of the 25 patients in the aneuploid group developed carcinomas. In terms of percentages, 3% of the normal group developed carcinomas as compared to 60% of the intermediate group and 84% of the abnormal group.

Time: As you would expect, the aneuploid group developed carcinomas faster than the others. The mean time to develop a carcinoma after the initial assessment for the aneuploid group was 35 months (ranging from 4-57) while in the intermediate or tetraploid group, it took 49 months (ranging from 8-78).

Survival: Once diagnosed and treated, the cumulative disease-free survival rate was 95% for the diploid or normal group, 40% for the intermediate or tetraploid group, and 18% for the abnormal or aneuploid group.

Smoking habits: While the smoking habits of 13 patients could not be verified, 27 of 137 subjects never used tobacco. A carcinoma developed in 5 of these 27 non-smokers. Twenty-two (22) out of the current 85 who smoked, developed carcinomas. Two (2) of the 13 whose tobacco use was unknown, also developed carcinomas.

Conclusions: The investigators felt that watchful waiting was appropriate for patients who have a normal (diploid) DNA content in their leukoplakia. However, those with abnormal (aneuploid) DNA content should be treated as true carcinomas. The pooled data from all three DNA ploidy groups resulted in 24% of all leukoplakias transforming into malignancies.

It was noted that high risk patients with previous cancers of the oral cavity, carcinomas in situ, cancers of the aerodigestive tract, or those with erythroplakia (which has a 90% occurrence of becoming malignant) were not included in this study. The incidence of secondary cancers for these patients is greater than those with a first-time lesion, and including them would skew the results.

Excisional biopsies were felt to be curative in some cases. The authors noted that all 6 aneuploid cases that did not develop into carcinomas (there were 4 original aneuploid subjects and two more that developed from the diploid/normal group as the study progressed) had excisional biopsies.

While the DNA content ploidy was a reliable prognostic marker for patients with leukoplakia, tobacco use was not. The study was unable to quantify alcohol consumption in these subjects and could not, therefore, exclude it as a contributing factor. Subtle genetic factors were thought to also contribute to the transformation of a white leukoplakic patch into a carcinoma.

Comment: The bottom line is that few white patches ever turn into squamous cell carcinomas. But when they do, the 5-year survival rate is poor. We recommend all white patches in the mouth be investigated by either brush biopsies or simply have them excised in toto.

*SudbŘ J., Kildal W., Risberg B., Koppang H.S., Danielsen H., and Reith A.: DNA content as a prognostic marker in patients with oral leukoplakia. N Engl J Med 344:1270-1278, 2001.

Remember your mother saying, "Chew your food slowly?"
Here's what she never knew

While mom may have been on target when we were kids, what would she say to those who have periodontal problems along with coronary artery disease or mitral valve prolapse (MVP)? Forget about how we masticate our food; is the mere act of chewing food deleterious to our health? In an abstract, silly way, (think of Jerry Seinfeld talking to George) "Swallowing…good; chewing…bad." But is that really so silly? Consider the following.

It is currently fashionable to hypothesize that having periodontal disease puts one at risk for patients with systemic disease. We fear that patients receiving dental treatment may have bacterial components unleashed into their bloodstream that will work their way into clogged coronary arteries or inhabit weakened mitral valves. In the former, as the theory goes, a patient might conceivably suffer a myocardial infarct. In the latter, the patient may succumb to subacute bacterial endocarditis (SBE). To prevent the former, patients are urged to receive periodontal treatment for their gum conditions. To prevent the latter, patients with MVP need to take oral antibiotics prophylactically 1 hour before each dental visit. So treatment helps in one case and prevention helps in the other; both allegedly save lives. This is what the dental schools teach. This is what we read in newspapers and magazines. This is how we practice. But should it be gospel?

While no one refutes the fact that bacteria can be introduced into the bloodstream during dental treatment, a group of researchers wanted to study something more benign and less aggressive than the everyday actions of toothbrushing, flossing, and even eating. They chose to study the systemic effects of chewing.*

Forty-two (42) subjects with 2 or more pockets > 5mm were used in this study. None of these patients had periodontal treatment during the previous two months nor had they taken an antibiotic during the three months prior to this study. Their results were compared to 25 control subjects who were free (no pockets >3mm) of periodontal disease. Baseline blood samples were taken from both groups to measure circulating endotoxins. Then new blood samples were drawn 5-10 minutes after each group chewed gum 50 times on each side of their mouth. Each assay for endotoxin was performed twice. In addition, a method was devised to correlate the patient's periodontal condition to the amount of circulating endotoxin found in their bloodstream.

Results: Endotoxin levels were found to increase in both the control and test groups after gentle mastication. However, the test group levels - those with periodontal pockets - were significantly higher than those of the controls. This evidence supports the hypothesis that periodontal disease can play a causative role in systemic pathologies by acting as a source for inflammatory bacterial components in the bloodstream.

Discussion: How can normal chewing, swallowing, and speaking put us at bacterial risk? The authors suggest any number of ways. For instance, when teeth rub together or there are occlusal pressures or there is a "pumping" effect of the tooth in the socket, each may allow bacterial access into our bloodstream through the ulcerated epithelium in our pockets. While the authors admitted many shortcomings to their study, the fact remained that patients with periodontal pockets did have a greater endotoxemia than did the healthy control patients. They suggested that their finding may be linked to previously published retrospective studies that reported a higher incidence of periodontal disease in patients with cardiovascular disease.

Our conclusions: The subtext of this study is that everyone who is at risk for cardiovascular disease should strive for optimum dental health. Good dental health reduces the numbers of circulating endotoxin in the bloodstream when we eat, chew, swallow, or talk. So when mom said, "Chew your food slowly" for digestive reasons, she wasn't thinking about long-term cardiovascular effects.

There's another issue this report avoids but is important to discuss. How necessary is it to premedicate patients for dental appointments with antibiotics (we know we must do this and are not recommending to stop) if they have MVP, hip and knee replacements, pacemakers, arterial shunts, or other medical devices implanted in their bodies? According to this paper, endotoxins enter the bloodstream not only when we eat, but when we chew gum, swallow (which we do 2,000 times/day) or even speak. Should people who need prophylactic antibiotics for dental appointments be taking them for daily living?

*Geerts S.O., Nys M., De Mol P., Charpentier J., Albert A., Legrand V., and Rompen E.H.: Systemic release of endotoxins induced by gentle mastication: association with periodontitis severity. J Perio 73:73-78, 2002.

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