Trisha E. O`Hehir, RDH, BS
Cigarette smoking may be the single most important environmental risk associated with periodontal disease. In the past, most of the information concerning smoking and gum disease was observational in nature. Clinically, smokers have higher levels of plaque and calculus, inadequate levels of home care, more bone loss, and more missing teeth than nonsmokers. Recently, the cell-level effects of smoking have been identified, and it is now clear that smoking affects periodontal structures both directly and indirectly.
Both the nicotine and heat of smoking affect physical defense mechanisms. The oral cavity temperature of smokers reaches 107.6 degrees F, resulting in alterations in the epithelial tissue and compromising the body`s defense mechanisms. Nicotine is capable of penetrating epithelial cells, inducing vascular changes in connective tissue, suppressing immunological defense mechanisms, and altering fibroblast functions - all leading to significant levels of bone loss.
Nicotine is rapidly absorbed into the bloodstream through the oral mucous membranes and into the pulmonary circulation through the lungs. Initial increases in blood-flow rates result from vasodilatation and remain high for five minutes after smoking. Within 10 minutes, blood-flow rates are lowered by nicotine, causing vasoconstriction of the blood vessels within the connective tissue. Reduced blood flow can last up to three hours after a single cigarette. Vasoconstriction results in reduced blood flow to the gingiva, reduced oxygen to the cells, reduced blood constituents, and a reduction in the capacity to remove cellular waste products from the gingiva.
Clinically, the vasoconstriction results in fibrous tissue without the customary bleeding upon probing that is associated with periodontal disease. In smokers, the lack of bleeding on probing does not indicate healthy tissue as it does in a nonsmoker.
In looking at the immune system, polymorphonuclear leukocytes (PMNs) are the first line of defense in an inflammatory response. These cells are capable of adhering to and ingesting target bacteria. When compared to nonsmokers, smokers have a 50 percent reduction in functional PMNs, leading to reduced phagocytic capability. The effect on PMNs is even more pronounced when a cigarette is smoked one hour before testing. The cell walls of these blood cells remain intact, but they no longer function effectively. These effects compromise the immune response to periodontal infection, as well as healing following periodontal therapy.
Nicotine initially will stimulate saliva flow, followed by a decrease in secretions, which directly affects the microflora of the mouth. This alteration may also be responsible for the higher levels of calculus found in smokers. Nicotine metabolites remain in the saliva and gingival crevicular fluid much longer than nicotine, continuing the active properties of nicotine.
Cotinine is an inactive breakdown product of nicotine. The half-life of nicotine following inhalation is approximately two hours. The half-life of cotinine is about 19 hours. Cotinine concentrations in the gingival crevicular fluid of smokers are five to six times higher than in salivary levels. This is not a surprise, since nicotine is known to easily penetrate skin and oral mucosa. On the other hand, cotinine is not detected in either saliva or gingival crevicular fluid of nonsmokers.
Fibroblasts are important cells in wound healing. Fibroblasts cultured in the presence of nicotine demonstrate a rapid and continuous uptake of nicotine over four hours of incubation. The nicotine is then released from the cells, but at a much slower rate than the rate of uptake. The presence of nicotine within the fibroblast cell is likely to disrupt normal cellular metabolic activity, such as collagen synthesis and protein secretion.
A laboratory study of fibroblast attachment to glass and root surfaces of extracted teeth suggests that nicotine may alter the nature of such an attachment, thereby interfering with the healing process following treatment. These microscopic alterations suggest that fibroblasts are not firmly attached. Instead, they demonstrated an increase in the number of attempted attachment sites. This phenomenon by the cells of OsearchingO for a potentially nicotine-free area leads to compromised healing.
We know smoking is the single most important contributing factor to periodontal disease. Understanding the cell-level effects may encourage us to become even more involved in the smoking cessation program in the office.
Trisha E. O`Hehir, RDH, BS, is a senior consulting editor of RDH. She also is editor of Perio Reports, a newsletter for dental professionals that addresses periodontics. The Web site for Perio Reports is www.perioreports.com. Her e-mail address is trisha@perioreports. com.
