The role of nicotine in bleeding

By Trisha E. O'Hehir

I have encountered quite a surprise! I've told you that nicotine causes vasoconstriction in continuing education courses and written about it in more than one previous column. For years, I believed the theory that nicotine causes vasoconstriction and that's why smokers with periodontal disease have less bleeding compared to non-smokers. It seemed a plausible explanation for the lack of bleeding in smokers.

Trouble is ... it was just a theory.

Even though it seemed to make perfect sense, it was never proven. That's right, there's no scientific evidence to support this well-accepted concept. You and I both need to continue reading research and posing questions for dental hygiene researchers.

Lacking scientific research to support this widely accepted concept ... it's time for some detective work. Why is there bleeding in the first place?

Pocket wall ulceration provides easy entry to underlying tissues and blood vessels. An increase in the number of blood vessels is triggered by periodontal infection. The looping and spiraling of these capillaries characterize changes in vessel length and diameter. Increased vascularization contributes to tissue destruction associated with periodontitis and may explain, in part, the increased bleeding we see.

If that's the case, why do smokers have less bleeding? Are the capillaries different in smokers? Not according to recent research done in Turkey. No blood vessel differences were evident in tissue biopsies taken during periodontal surgery from smokers and non-smokers.

Typically we see puffy, red, bleeding gums and ulcerated pocket walls with periodontal disease, but not in smokers. Maybe some have puffy, bleeding gums, but most don't. Instead, they have pockets and bone loss, but the tissue is pink, fibrous and doesn't bleed easily on probing. Perhaps the fibrous tissue also lines the pocket wall, explaining the reduced bleeding upon probing. Right now, we still don't know.

We do know that when smokers with periodontal disease stop smoking, they start bleeding more. Researchers in London monitored bleeding in a group of patients enrolled in a smoking cessation program. These patients showed increases in gingival bleeding. To measure just the effects of smoking on bleeding, they told study subjects to continue their daily brushing and flossing habits without change. The researchers didn't want changes in oral hygiene to influence the results. Despite these instructions, plaque scores dropped considerably. It seems just being in the study may have motivated participants to do a better job of brushing. That's the "Hawthorne Effect," and it occurs quite often with clinical studies. Despite lower plaque scores after a month, bleeding scores were increased twofold, going from 16 percent of sites to 32 percent of sites.

You can now quote research for what you've known all along — quitting smoking leads to increased bleeding.

Knowing this, be sure to inform your patients who want to quit smoking that they may see an initial increase in gingival bleeding when they quit. This increase in bleeding confirms the reversibility of the effects of smoking. As their body recovers from the effects of smoking, they will eventually be able to eliminate the bleeding.

Let's go back to the vasoconstriction theory. In 1947, Dr. Pindborg published his hypothesis that the nicotine in cigarettes could act directly on the blood vessels of the gingivae — causing vasoconstriction — thus explaining why smokers exhibited less bleeding with periodontal disease than non-smokers. The reduced blood flow would decrease the number of blood cells and the amount of oxygen reaching the tissue. Fewer blood cells and less cytokine destruction of the tissue would explain the lack of puffy, bleeding gums. Vasoconstriction would also reduce the ability to remove toxins and waste products from the area, explaining bone loss. It seemed to make perfect sense; but it was never proven scientifically.

In an attempt to document vasoconstriction caused by nicotine, researchers monitored heat related to gingival blood flow in a rabbit.

I can just picture it: perio grad students — white lab coats flapping — out behind the dental school teaching the rabbit how to smoke. Probably not. I'm sure they figured out some contraption to force smoke into the rabbit's mouth or another way to deliver nicotine, since they did show blood-flow changes related to nicotine.

They showed vasodilation first, or rather increased blood flow, which they assumed to be vasodilation. They also measured a decrease in blood pressure. Within 10 minutes, these effects were reversed. The reduced blood flow they measured was assumed to be vasoconstriction. Not very strong research to support the vasoconstriction theory.

Laser Doppler technology more accurately measures blood cells and blood flow. Readings are based on shifts in back-scattered laser light measured through both skin and gingivae. Researchers in London used this technology to measure blood flow in maxillary interdental papilla and on the forehead of subjects during and after smoking. The light smokers were the only ones to show a change in blood flow, and it wasn't a decrease. They showed an increase in blood flow during and after smoking. Non-smokers and heavy smokers didn't demonstrate a significant change in either gingival or forehead blood flow.

Other researchers have also shown an increase in blood flow during and after smoking, which they related to increased blood pressure and heart rate. Researchers looking at blood flow have not been able to show any vasoconstriction caused by smoking. Instead, reduced bleeding in smokers with periodontal disease is probably due to complex interactions of the 6,000 chemicals found in cigarettes and the heat produced by smoking. For whatever reason, the pocket wall is less ulcerated, and thus less likely to puncture and bleed upon probing.

The exact mechanism has yet to be determined. Perhaps with the magnified, direct vision of Perioscopy, the pocket walls of smokers can be compared to those of non-smokers to explain this phenomenon. This is just one of many concepts in dental hygiene that needs to be addressed by scientific research. Be an oral health detective and keep asking why.

Trisha E. O'Hehir, RDH, BS, is a senior consulting editor of RDH. She is also an international speaker, author, instrument designer, inventor, and oral health detective. Her Web sites are and She can be reached at (800) 374-4290 or at

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