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Notes: Abstract. This paper examines the effects of smoking on the treatment outcomes of two nonsurgical therapies: (1) scaling and root planing alone (SRP) or (2) controlled-release of subgingivally delivered doxycycline hyclate in a polylactic acid based polymer gel. Subjects from 2 9-month multicenter studies were classified as nonsmokers (never smoked: 100 subjects), former smokers (137 subjects), and current smokers (≥10 cigarettes/day: 121 subjects). Clinical parameters were analyzed for treated sites with baseline probing depths ≥5 mm and for a subset of treated sites with baseline probing depths of ≥7 mm. Clinical parameters (plaque levels, clinical attachment levels, pocket depths, and bleeding on probing) were analyzed at baseline, 4, 6, and 9 months. In the doxycycline treated group in general, there were neither marked significant differences in clinical attachment gain nor differences in probing depth reduction among the 3 smoking groups. On the other hand, in the scaling and root planing treated group in general, there were significant differences in clinical attachment gain and pocket depth reduction, with non-smokers responding better than former smokers and current smokers at 6 and 9 months. These differences in clinical response between scaling and root planing alone versus controlled-release of locally-delivered doxycycline hyclate among these 3 smoking groups are discussed in relation to treatment implications for smokers.

Notes: The periodontal syndrome in the rice rat was studied in animals fed a high sucrose diet. Progressive degenerative and inflammatory changes within the coronal aspects of the rice rat psriodontium (viz. sulcus, epithelium and lamina propria) were noted. PMN's were seen to migrate from blood vessels within the lamina propria, through the basal lamina, and to either the cemental surface or to the bacterial plaque, where a minimal degree of PMN phagocytosis and degranulation was observed. The degree of PMN phagocytosis appeared to be inversely related to the density of bacterial plaque as viewed on the electron microscopic level.Progressive degenerative changes (viz. vacuolization, lipid accumulation, mitochondrial swelling, etc.) were seen in gingivai epithelial cells subjacent to the bacterial plaque, as well as at the basal layer. Similar changes were noted in fibroblasts in the underlying lamina propria. At later stages of observation (8–14 weeks post-weaning) a prominent population of macrophages and mononuclear cells was seen within the lamina propria. “Clumping” of these cell types with degenerating fibroblasts was a common finding.

Notes: In this study on the periodontal syndrome in the rice rat, the progressive inflammatory and degenerative changes were noted in the transseptal fiber area and alveolar crest.The predominant inflammatory cell types within the transseptal fiber area were PMN's, monocytes and macrophages. Progressive degenerative changes were noted in fibroblasts and collagen fibers with replacement of these elements by the inflammatory infiltrate.At the alveolar crest, extensive osteoclastic activity was observed. Expressions of this activity included the presence of prominent osteoclast ruffled borders and osteoclastic phagocytosis of osteocytic cells. Degenerative changes within osteoblasts were noted at later stages.From these observations, the accelerated rate of destruction seen in this animal model can be explained in part by the increase in resorptive elements (macrophages, osteoclasts) with the simultaneous decrease in formative elements (epithelial cells, fibroblasts, osteoblasts).

Notes: Tobacco smoking is a major risk factor in the incidence and severity of periodontal diseases. Alterations of neutrophil function by short-term high levels of smoke during the act of smoking (acute smoke exposure) as well as long-term exposure to lower levels of tobacco substances in the bloodstream (chronic smoke exposure) may play a role in the pathogenesis of periodontal diseases in smokers. The polymerization and depolymerization of f-actin in response to infectious agents or inflammatory mediators is a critical process in a variety of neutrophil functions. In this study, we examined the effects of in vitro smoke exposure on neutrophils from smokers and non-smokers (which may be comparable to in vivo acute smoke exposure) and neutrophils from smokers not exposed to further in vitro smoke (which may be comparable to chronic smoke exposure) on f-actin kinetics. Peripheral neutrophils were isolated from seven healthy smoking subjects and seven healthy age-matched non-smoking subjects and exposed to 1–5 min of acute smoke in a smoke box system or not exposed to further smoke (baseline controls). Selected aliquots of neutrophils from control and 5-min exposures of acute smoke were then stimulated with the chemotactic peptide F-met-leu-phe at 10−7m for an additional 30–360 s. Cells were fixed and permeabilized, stained for f- actin with NBD phallacidin, and analyzed by flow cytometry. From baseline to 5 min of invitro smoke exposure, there was a 38% decline in f-actin stain in non-smokers and a 30% decline in f-actin stain in smokers ( p 〉 0.05) with f-actin values slightly higher in smokers than-non-smokers ( p 〉 0.05). With F-met-leu-phe stimulation, both smokers and-non-smokers demonstrated a characteristic rise in f-actin stain from 0 to 120 s with a subsequent decline to baseline at 360 s and no significant differences in f-actin levels at any time of stimulation between groups. After preincubation with 5 min of in vitro smoke, the magnitude of rise in f-actin was less in both smokers and non-smokers when compared to cells not incubated with 5 min of smoke ( p 〈 0.05 at 120 s for both smokers and non-smokers). F-actin values in smokers were higher than-non-smokers from 30 to 360 s of F-met-leu-phe exposure ( p 〉 0.05). These results demonstrate that in vitro smoke exposure may impair normal f-actin kinetics. These alterations in f-actin kinetics may in turn affect other neutrophil functions which may impact on the pathogenesis of periodontal diseases in smokers.

Notes: In this study on the periodontal syndrome in the rice rat, observations were made on rice rats fed stock diet and followed from six days to fifteen weeks after birth, and on rice rats fed a high sucrose diet (Diet 700) from weaning (3 weeks after birth) and followed to seventeen weeks after birth.In rats fed stock diet, early massive accumulations of bacterial plaque were seen on erupting posterior teeth with an underlying PMN exudate and a PMN infiltrate within the gingival epithelium and lamina propria. Inflammatory and resorptive changes were rarely seen in the transeptal fiber area and alveolar crest in this group of animals.In rats fed diet 700, similar patterns of bacterial plaque accumulations and PMN infiltrations were seen. At later time periods, this PMN infiltrate was commonly seen to extend through the transseptal fiber area to the alveolar crest where marked osteoclastic activity was noted. Such apical extension of the inflammatory infiltrate was associated with ulceration of the overlying gingival epithelium.

Notes: Alterations in neutrophil functions by both chronic low levels of tobacco and by acute short-term higher levels of tobacco smoke, as encountered during the act of smoking, may play a role in the pathogenesis of periodontal diseases in smokers. Among the early migration events of neutrophil function is the alteration in surface expression of L-selectin and the CD11/18 integrins. In the present study we examined the effect of in vitro smoke exposure and nicotine alone on the expression of these 2 adhesion molecules in neutrophils from smokers and non-smokers. We also determined the physiological relevance of this in vitro system by assessing the levels of nicotine exposure in this in vitro system and comparing these levels to acute and chronic levels of nicotine in saliva and gingival crevicular fluid. Peripheral neutrophils were isolated from the blood of smokers (〉 1 pack/d) and non-smokers and incubated in vitro with either cigarette smoke (0–5 min), 10−7 M F-met-leu-phe, or nicotine alone at 1.62mg/ml to 162ng/ml (10−2 M-10−6 M). The neutrophils were then incubated with fluoresceine conjugated anti-Leu8 (L-selectin), anti-CD18 (CD18 integrin), or γ-4 (non-specific control), fixed and analyzed by flow cytometry. With cigarette smoke exposure, there was an approximate 75% shedding of L-selectin in both smokers and non-smokers with no marked difference between groups at 1–5 min of smoke exposure. Cigarette smoke exposure resulted in a 15–20% increase in CD 18 expression in both smokers and non-smokers. At all time points, there was slightly greater but statistically insignificant expression of CD18 integrin in non-smokers when compared to smokers. These patterns of CD18 increases and L-selectin shedding were similar in magnitude to incubations with 10−7 M F-met-leu-phe. Acute smoke exposure resulted in elevation of nicotine in the smoke box to 529 ng/ml at 5 min, in saliva from 109.2 ng/ml before smoking to 1821.4 ng/ml after smoking, and in gingival crevicular fluid to 5961 ng/ml after smoking. No significant alterations in L-selectin or CD 18 expression were noted with in vitro nicotine from 1.62 mg/ml to 162 ng/ml.

Notes: Alterations in neutrophil functions by both chronic low levels of tobacco and by acute short-term higher levels of tobacco smoke, as encountered during the act of smoking, may play a role in the pathogenesis of periodontal diseases in smokers. Among the early migration events of neutrophil function is the alteration in surface expression of L-selectin and the CD11/18 integrins. In the present study we examined the effect of in vitro smoke exposure and nicotine alone on the expression of these 2 adhesion molecules in neutrophils from smokers and non-smokers. We also determined the physiological relevance of this in vitro system by assessing the levels of nicotine exposure in this in vitro system and comparing these levels to acute and chronic levels of nicotine in saliva and gingival crevicular fluid. Peripheral neutrophils were isolated from the blood of smokers (〈 1 pack/d) and non-smokers and incubated in vitro with either cigarette smoke (0-5 min), 10−7 M F-met-leu-phe, or nicotine alone at 1.62 mg/ml to 162 ng/ml (10−2 M-10−6 M). The neutrophils were then incubated with fluoresceine conjugated anti-Leu8 (L-selectin), anti-CD 18 (CD 18 integrin), or γ-4 (non-specific control), fixed and analyzed by flow cytometry. With cigarette smoke exposure, there was an approximate 75% shedding of L-selectin in both smokers and non-smokers with no marked difference between groups at 1-5 min of smoke exposure. Cigarette smoke exposure resulted in a 15-20% increase in CD18 expression in both smokers and non-smokers. At all time points, there was slightly greater but statistically insignificant expression of CD 18 integrin in non-smokers when compared to smokers. These patterns of CD 18 increases and L-selectin shedding were similar in magnitude to incubations with 10−7 M F-met-leu-phe. Acute smoke exposure resulted in elevation of nicotine in the smoke box to 529 ng/ml at 5 min, in saliva from 109.2 ng/ml before smoking to 1821.4 ng/ml after smoking, and in gingival crevicular fluid to 5961 ng/ml after smoking. No significant alterations in L-selectin or CD 18 expression were noted with in vitro nicotine from 1.62 mg/ml to 162 ng/ml.

Notes: In this paper on the periodontal syndrome in the rice rat, the effects of dietary penicillin and tetracycline on the progressive inflammatory and degenerative changes (as seen in rice rats fed diet 700 alone) were noted at the light and electron microscopic level. Throughout the observation period (0–14 weeks postweaning), animals fed diet 700 with penicillin or diet 700 with tetracycline showed no evidence of bacterial colonization, a minimal PMN infiltrate restricted to the gingival epithelium and subjacent lamina propria, and no marked degenerative changes within cells that normally inhabited the periodontium (viz. epithelial cells, fibroblasts, osteoblasts). Marked osteoblastic or osteoclastic activity was rarely noted along the alveolar crest in this group of animals.These results give added support to the concept of a single microbial agent or group of microbial agents, as the primary etiology of this disease.