This paper presents the acute effects of cigarette smoking on blood flow to the gingiva in 12 young smokers. Relative gingival blood flow (GBF) was measured by a laser Doppler fiberoptic probe placed 1 mm into the buccal sulcus of tooth no. 26. The probe continuously measured the flux of blood cells (velocity X number of cells) in the gingival crest. Relative skin blood flow (SBF) to the forearm and heart rate were also monitored continously; blood pressure (BP) was assessed at 5-min intervals. After resting for 5 min, subjects sham smoked an unlighted cigarette for 5 min, then smoked the cigarette, and finally rested for 25 min afterwards. Mean changes from resting for all variables were compared to sham smoking for each 5 min block. Mean GBF rose significantly above sham smoking values during smoking, and remained elevated during the first 5 min after smoking (p less than 0.05). Mean SBF decreased slightly during and after smoking, but the changes were not significantly depressed compared to sham smoking (p greater than 0.05). During smoking, BP and heart rate increased significantly over sham smoking (p less than 0.05). GBF increased almost linearily when the probe was placed into the gingival sulcus; this phenomenon did not occur when the probe was placed externally to the gingival crest. The theory that smoking impairs gingival blood flow may not be true in humans.

For more than 20 years, investigators have unanimously agreed that human periodontitis is caused by bacterial colonization of the surfaces of the teeth and their extension apically. Recently, several investigators have demonstrated that most, if not all, individuals manifesting the early-onset, aggressive forms of periodontitis have abnormalities in their peripheral blood phagocytes which can be detected as abnormal cell motility or adherence. Because of the major role of these cells, especially the neutrophilic granulocytes, in host defense against the microbial onslaught at the gingival sulcus, these leukocyte abnormalities have been considered to be the major determinant of susceptibility to microbial infection and invasion of the periodontal tissues. In recent years the possibility that other etiologies may be involved has not been seriously considered. The purpose of the present communication is to focus attention on the idea that factors other than bacteria and host defense mechanisms may be of significance. We specifically want to call attention to a potentially important role for root cementum.

Previous studies of gingival blood flow have used techniques that were discrete, invasive, or only applicable to animals. The present study assessed this parameter in 10 healthy humans using a noninvasive laser Doppler flowmeter (LDF). Blood flow rate was determined in the interdental papillae, free and attached gingiva, and alveolar mucosa. Measurements were made continuously at four sites per patient and discontinuously at 21 sites per arch representing the four locations. The effects of heat, cold, pressure, and occlusal force on blood flow were measured. Blood flow wave patterns differed consistently by tissue type. Mean blood flow was significantly higher (p

This study tested the effectiveness of a rechargeable electric toothbrush, Interplak, in removing supragingival plaque and resolving gingivitis. Forty adults with gingivitis were randomly assigned to either a "manual" or "electric" group. Detailed oral hygiene instructions were given and a blind examiner assessed plaque scores before and after brushing, toothbrush abrasion, and gingival inflammation at baseline, 1, 2, and 4 weeks. Subjects using the electric brush had significantly lower (P less than 0.05) mean plaque and gingival inflammation scores. The electric group's plaque scores fell from 77% at baseline to 28% (before brushing) and 14% (after brushing) at 4 weeks; the manual group's dropped from 75% to 50% and 30% (before and after brushing, respectively). The mean G.I. for the electric group fell from 1.65 at baseline to 1.28 at 4 weeks, while the manual group's scores decreased from 1.65 to 1.43. The results suggest that the electric brush removed supragingival plaque and resolved gingivitis better than the manual brush over a 28-day period. However, a telephone survey conducted 6 months later indicated that most subjects were not using the device twice a day as they had during the study.

In a previous publication, we described the clinical and radiographic findings of a family in which the children manifested premature exfoliation of the deciduous teeth. We now report for the same family the results of extensive laboratory studies performed on blood and urine, analysis of periodontal microflora, and a family pedigree. We demonstrated the presence of putative periodontal pathogens in the subgingival microflora, elevated levels of serum antibodies reacting to Bacteroides gingivalis, Capnocytophaga gingivalis, and C. sputigena in 2 of the children, and significantly suppressed monocyte chemotaxis in all 3 children. Phosphoethanolamine was found in the urine of the father and all 3 children, but not in the mother. Likewise, serum alkaline phosphatase was abnormally low for all 3 children, and was at the extreme low end of normal range for the father, but was normal for the mother. On the basis of the alkaline phosphatase and phosphoethanolamine measurements, we assigned a diagnosis of hypophosphatasia to the 3 children. Phosphoethanolamine and alkaline phosphatase were also abnormal in the paternal grandmother and her brother. The son of this brother who was deceased had a daughter manifesting premature loss of the primary teeth. The data are consistent with an autosomal dominant mode of transmission. In the light of our findings, hypoplastic cementum must be considered in the etiology of some forms of early-onset periodontitis.

Several studies have documented suppressed polymorphonuclear neutrophil (PMN) chemotaxis in most patients with juvenile periodontitis. In contrast, data regarding PMN chemotaxis in patients with rapidly progressive periodontitis are very limited, and monocyte (MN) chemotaxis and random migration of PMNs or MNs from these patients have not been studied previously. Accordingly, we examined cell motility of PMNs and MNs from 27 patients with rapidly progressive periodontitis, 5 patients with juvenile periodontitis, and 37 normal control subjects by using a microchamber technique and the synthetic peptide N-formylmethionyl-leucyl-phenylalanine (FMLP) as the chemoattractant. As a group, PMNs and MNs from patients with rapidly progressive periodontitis manifested significantly enhanced random migration relative to control cells (P less than 0.001), suppressed directed migration (chemotaxis) at FMLP doses of 10(-9) and 10(-8) M (P less than 0.05), and enhanced directed migration at a dose of 10(-6) M FMLP (P less than 0.01). In contrast, PMNs from patients with juvenile periodontitis exhibited normal random migration, and directed migration was significantly suppressed at all doses of FMLP tested (P less than 0.05). An abnormality of either PMN or MN motility was observed in 26 of 27 patients with rapidly progressive periodontitis. Enhanced random migration was seen in PMNs in 63%, MNs in 39%, and both cell types in 26% of the patients. Suppressed chemotaxis was seen in PMNs in 85%, in MNs in 74%, and in both cell types in 69% of the patients. The prevalence and magnitude of abnormalities in motility were somewhat lower in treated than in untreated patients. Thus, most, if not all, of this subgroup of patients with early onset, highly destructive periodontitis have abnormalities in PMN or MN motility, and these defects may differ from those seen in cells from patients with the juvenile form of the disease.

No abstract

No abstract