This study examined the effect of nicotine on fibroblast attachment to glass and nondiseased human root surfaces. Human foreskin fibroblasts (HFF) were trypsinized, suspended in RPMI 1640 medium, and incubated with autoclaved human root sections and nicotine concentrations of zero (control), 25, 50, 100, 200, or 400 ng/ml. The root sections were examined for fibroblast attachment at 24, 48, and 72 hours by light microscopy and scanning electron microscopy (SEM). Additional trypsinized HFF were incubated on glass surfaces with the same concentrations of nicotine and examined at one week by light microscopy. HFF attached and grew on glass and root surfaces at all concentrations of nicotine. Controls on glass surfaces exhibited a normal monolayer of long spindle‐shaped fibroblasts with a parallel alignment and minimal overlapping. Nicotine‐treated HFF exhibited a haphazard arrangement with cell overlapping and vacuolization of the cytoplasm. Under SEM, the controls had smooth surfaces and appeared firmly attached to the root surface via (1) microvilli and filopodia on the cell boundaries and (2) short, branched, thinto‐medium width cytoplasmic processes with microvilli and filopodia on their boundaries. Few microvilli were noted on the control cell surfaces. HFF exposed to nicotine had microvilli and filopodia on the cell surfaces and long thin and long broad cytoplasmic processes with many microvilli and filopodia that projected away from the root surface. These findings suggest that the nature of fibroblast attachment to glass and root surfaces is altered by nicotine. A similar disturbance in fibroblast attachment may occur in humans who use nicotine‐containing products, making them more susceptible to destruction of the periodontium and less responsive to new attachment after periodontal therapy.

A study was undertaken to determine the presence of cotinine, a metabolite of nicotine, in the saliva and gingival crevicular fluid of smokers with periodontal disease. Saliva and crevicular fluid samples were obtained from 16 habitual cigarette smokers and analyzed by High Performance Liquid Chromatography (HPLC) for the presence of cotinine. Thirteen non–smokers with periodontal disease served as controls. There was no evidence of cotinine (within our detection levels) in either the saliva or crevicular fluid of any of the non–smokers. Cotinine, in a wide range of concentrations, was detected in the saliva and crevicular fluid in all of the 16 cigarette smokers. The presence of a nicotine metabolite in the saliva and gingival crevicular fluid reflects the extent of the systemic distribution of nicotine in smokers. The vasoactive properties of nicotine are well known and may possibly affect the pathogenesis of periodontal disease.

There is a growing body of scientific evidence to support the concept that the use of tobacco products significantly contributes to the progression of periodontal disease or is detrimental to healing following periodontal therapy. Several studies have shown toxic effects of nicotine on peripheral circulation and the immune response. The purpose of the present study was to identify and compare the quantity of nicotine present on root planed and nonroot planed surfaces of teeth from smokers. Twenty-nine single-rooted teeth from 11 smokers were extracted, brushed clean, and the roots sectioned longitudinally. The respective halves were either left untreated (Group A) or thoroughly root planed (Group B). Pulpal tissue was removed and the individual root sections weighed. Each half was extracted for nicotine using a methylene chloride technique. Quantification was performed using high pressure liquid chromatography (HPLC) and the sections compared on a nicotine per root weight basis. Results showed a greater amount of nicotine present on non-root planed sections than on treated sections, although some treated specimens revealed small amounts of the substance. These findings suggest that nicotine is present on the root surface but is largely removed by thorough root planing. Its presence is not surprising in light of the recent finding that nicotine and cotinine, the major metabolite of nicotine, are found in gingival crevicular fluid. Recent studies have shown a particularly harmful effect of nicotine on fibroblasts. Its presence on root surfaces may, therefore, impair wound healing and alter the host response in periodontal disease. The use of tobacco products in conjunction with periodontal therapy may interfere with optimal healing and/or lead to further periodontal breakdown.

This study showed that the nature of cell attachment to either glass or root surfaces is altered by nicotine, and marked detachment was noted when nicotine exposure was coupled with vigorous agitation at different rpm. Marked detachment noted in all specimens at 200 rpm indicates that this speed is excessive for use in subsequent experimentation.

The purpose of this study was to assess the value of ultrasound in the measurement of periodontal bone morphology. Four patients scheduled for periodontal surgery were selected for the study. The Ocu-Scan 400 machine was used and adjusted according to the manufacturer's instructions. Teeth involved in the study were measured on the facial aspect at three different points: mesial, midfacial and distal (except one tooth measured only at the mesial point). Two different presurgical measurements were made with the use of ultrasound. The distance between the gingival margin and the crest of alveolar bone was measured during the surgical procedure. No correlation could be made between the different measurements obtained. From the results the following was concluded: measurement of alveolar bone topography with the presently available ultrasound probe is not accurate, and ultrasound measurement is a fast and painless procedure.