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

{"title":"Osteoporosis and periodontal disease: is there a relationship?","authors":"C B Krejci","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Osteoporosis, by definition, is a generalized progressive reduction in both bone mineral and bone matrix which results in bone of normal composition but decreased mass. Functionally, osteoporotic bone is characterized by greater fragility and an increased propensity to fracture. It ranks as the most common metabolic bone disease and the most common skeletal disorder in the world. As such, it constitutes a major public health problem. Due to the extent of the disease, many have questioned its relevance to the maxilla and mandible and its possible relationship to periodontitis. The purpose of this paper is to review both osteoporosis and periodontitis and to present the research completed to date which has investigated the possible interrelationships between the two diseases.</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"44 2","pages":"37-42"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20403753","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontal disease, diabetes, and immune response: a review of current concepts.","authors":"D A Grant-Theule","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A reasonable interpretation of the present evidence indicates that diabetes, when a complication of periodontitis, acts as a modifying and aggravating factor in the severity of periodontal infection. Diabetics with periodontitis who were young and poorly controlled, those who were long-duration diabetics, especially those over 30 years old, demonstrated more attachment loss, bone loss, and deeper probing pocket depths than their nondiabetic controls. It seems that the earlier the onset of diabetes and the longer the duration, especially without consistent control, the more susceptible the individual will be to periodontal disease. Consequently, once a diabetic contracts periodontal disease, it is usually more destructive. Although plaque scores of diabetics may be comparable to or even less than those of nondiabetics, diabetics often exhibit higher gingival index scores. The elevation of this particular clinical parameter is indicative of the microangiopathy associated with diabetes. Diabetic microangiopathy contributes to compromised delivery of nutrients to surrounding tissues and poor elimination of metabolic waste products. The complications associated with diabetes such as macroangiopathy, microangiopathy (i.e., retinopathy), ketoacidosis, and hyperglycemia result in impaired wound healing, immunosuppression, and susceptibility to bacterial infection. Individuals ages 30 to 40 suffering from diabetic retinopathy had significantly more gingival inflammation than controls or diabetics without complications. Collagen metabolism is defective in diabetics and is one component underlying delayed wound healing. Animal studies have been instrumental in elucidating the details of delayed wound healing. Hyperglycemia was associated with increased collagenase and protease activity in the gingiva of rats. Vascular wound healing in rats, particularly new re-endothelialization across vascular anastomoses, was significantly impaired. Diabetic abnormalities in immune response include impaired neutrophil chemotaxis, phagocytosis, and adhesion. Decreased neutrophilic chemotactic response seems to be attributable to protein factors in diabetic serum that competitively bind neutrophil receptors, thereby preventing complement-mediated phagocytosis. Because diabetics are not able to eliminate circulating immune complexes (CIC) effectively, serum CIC levels are elevated. There are microbiological differences in the characteristic flora of NIDDM patients and IDDM patients with periodontitis. These differences are not associated with diabetic impaired immune response. Ultimately, bacterial plaque is the primary etiology of periodontal diseases. Evidently, the host's response to bacterial plaque and ability to heal following surgery is altered by diabetic disease. Therefore, a thorough history regarding onset of diabetes, duration, and diabetic control would prove useful in the clinical management of diabetics presenting for treatment of periodontal disease.</p","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"44 3","pages":"69-77"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20403633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms of stimulus transmission across dentin--a review.","authors":"D G Gillam","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"43 2","pages":"53-65"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19511379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone growth factors: potential for use as an osseointegration enhancement technique (OET).","authors":"S Koka,&nbsp;J B Vance,&nbsp;G I Maze","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"43 3","pages":"97-104"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20170395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Root coverage techniques: a review.","authors":"V J Tackas","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"43 1","pages":"5-14"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19511378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Observations on the recurrence of destructive periodontal disease during a period of four years after treatment.","authors":"P N Galgut","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"43 4","pages":"137-45"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20170396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human dental plaque formation on plastic films. A quantitative SEM study.","authors":"M Brecx,&nbsp;M Winkler,&nbsp;L Netuschil","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"42 3","pages":"77-80"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19512846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"On passive eruption.","authors":"H N Newman","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"42 2","pages":"41-4"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18929170","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combination of tetracycline and metronidazole in the treatment and control of refractory periodontitis.","authors":"F A Khatiblou","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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).</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"42 1","pages":"5-8"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19058494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lack of evidence for hypophosphatasia as a factor in the pathogenesis of early-onset periodontitis.","authors":"E E Machtei,&nbsp;A Ben-Yehouda,&nbsp;Y Zubery,&nbsp;B A Sela","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":76686,"journal":{"name":"The Journal of the Western Society of Periodontology/Periodontal abstracts","volume":"42 4","pages":"113-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19511377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}