The Journal of the Western Society of Periodontology/Periodontal abstracts最新文献

Several investigators have demonstrated that intradental A-type (A beta and A delta) nerve fibers are responsible for the sensitivity of dentin and that the endings of the responding fibers are located in the pulp-dentin area of the tooth. The exact mode of transmission of stimuli (e.g., thermal, chemical, mechanical, etc.) across dentin, however, is still unclear, although several hypotheses have been proposed. These include direct nerve stimulation, dentinal receptor (transducer/modulation), hydrodynamic, and direct ionic diffusion hypotheses. Currently, the most accepted mechanism of intradental nerve activation associated with dentin sensitivity appears to be hydrodynamic in nature, although alternative mechanisms of transmission (e.g., direct ionic diffusion) cannot be ruled out. Recent investigations (in the cat), however, appear to provide evidence substantiating the hydrodynamic hypothesis.

Gingival recession with the exposure of root surfaces is a significant treatment problem facing the clinician. Controversy relative to treatment continues and centers primarily around the need for gingival width augmentation. In 1972, Lang and Löe advanced the concept that a true minimal width of keratinized gingival tissue was necessary for health. They showed that all surfaces with less than 2 mm of keratinized gingiva exhibited clinical inflammation and varying amounts of gingival exudate. In contrast, 80% of the surfaces with more than 2 mm of keratinized gingiva were clinically healthy, and 76% of these same surfaces failed to show gingival exudate. Since 1972, the majority of studies have found that minimizing inflammation is sufficient to maintain attachment levels, even in the absence of "adequate" widths of keratinized and attached gingiva. Certain situations may enhance recession, such as subgingival restorations and toothbrushing trauma, but if inflammation is controlled and the etiology eliminated, minimal amounts of keratinized gingiva can be maintained in a state of health without further recession. Such findings have led to the current concept that deemphasizes a need for gingival augmentation surgery when there is no accompanying need for root coverage. A requirement for root surface coverage arises when gingival recession has esthetic implications, where exposure has resulted in root sensitivity, or where recession complicates routine home care procedures. While agreement exists relative to the indications for root coverage, there are a variety of surgical techniques that can accomplish this end. The purpose of this paper is to review these techniques and to examine the indications for choosing one procedure over another.

The upper and lower extreme percentiles of change in clinical variables were analyzed for a period of four years after completion of periodontal therapy in order to assess the patterns of disease recurrence after treatment. This analysis has demonstrated periods of healing and relapse of sites within individuals, among different individuals, and among different clinical assessment variables utilized. As not all of the sites within different individuals heal or relapse at the same rate, the random asynchronous burst model of pathogenesis seems appropriate to incorporate the different clinical assessment parameters and different sites in different individuals simultaneously. Long-term recession and pocketing, however, may demonstrate opposite trends, giving the erroneous interpretation that attachment levels remain constant with time, whereas, in fact, an active "dynamic equilibrium" of tissue remodeling is established. A statistical model based on the dynamic equilibrium concept would enable account to be taken of the multifactorial interactions that incorporate site and subject interrelationships between different clinical assessment parameters. The dynamic equilibrium model may be suitable therefore as the basis on which statistical analysis of the progression of periodontal disease may be considered. However, as the value of this or other models of the periodontal disease process have not been established, the analysis of data to derive meaningful conclusions from complex statistical techniques may be premature.

The initial colonization of bacteria in previously clean teeth or artificial surfaces inserted in mouth has been reported to occur at various periods of time. Rönström et al., using light microscopy, saw that bacteria were present 10 seconds after prophylaxis. Bacterial culture studies have shown that microorganisms associated with the surface coating on tooth surfaces appeared within minutes after prophylaxis. Furthermore, Rönström et al. noted that the number of bacteria increased over a period of four hours. In contrast, ultrastructural investigations of early plaque have demonstrated bacterial colonization only within the first two hours of plaque development in a few samples obtained on a smooth surface and in most samples on a rough surface. However, microorganisms have been found regularly after four hours of plaque accumulation in subjects with healthy gingiva. The aim of the present investigation was to determine the earliest occurrence of bacterial colonization in situ and to observe the pattern of the initial formation of human dental plaque.

Nine patients with refractory periodontitis were selected for this study. Each patient had undergone surgery once or twice in the previous five years and had been on three-month recall for clinical examination and scaling. During the maintenance phase of therapy and despite regular scaling, each patient had additional pocket formation that was either localized or generalized. Pocket depths in each patient were recorded and scaling was carried out. Three months later the patients were examined, and again no improvement was observed in the pocket depths. This time all patients were scaled again, and 250 mg tetracycline every six hours for 20 days as well as 250 mg metronidazole every eight hours for seven days were systemically administered. After an additional three months, patients were again examined and pocket depths measured. The latter examination disclosed that the clinical condition of the gingiva, as shown by bleeding and exudate, had improved. The pocket depths had also been reduced. The scaling-alone mean pocket depths were 4.93 mm, whereas the scaling-plus-antibiotic measurements were reduced to 2.78 mm. The difference was significant (p = 0.01).

Hypophosphatasia, an inheritable metabolic disorder affecting calcification, has been shown to have various oral manifestations. Recently, it was suggested that it may serve as a predisposing factor in the pathogenesis of early-onset periodontitis. The present study was designed to examine the frequency of hypophosphatasia among patients with juvenile periodontitis and rapidly progressive periodontitis. Eighteen patients, nine females and nine males (age 19-37 years, mean 23.2 years), were included in this study. Venous blood and urinary samples were collected and assayed for alkaline phosphatase and urinary phosphoethanolamine. Mean alkaline phosphatase levels (109 +/- 35 IU/L) were within the normal limits for all patients except one who exhibited slightly lower than normal values. Urinary phosphoethanolamine, a typical marker of hypophosphatasia, was absent from all specimens, which rules out the possible diagnosis of such disorder in these patients. Until more information is available, the role of hypophosphatasia as a predisposing factor in early-onset periodontitis is yet to be established.