The enamel matrix derivative (EMD) has been recently introduced in the periodontal field to overcome short-comings associated with currently available regenerative techniques. Information accumulated over the past years with application of EMD guided regeneration (EGR) in intrabony periodontal defects allowed a thorough evidence-based retrospective analysis. Clinical data from EMD controlled studies were pooled for meta-analysis and weighted according to the number of treated defects. Clinical attachment gain amounted to 3.2 +/- 0.9 mm (33% of the original attachment level) and probing reduction averaged 4.0 +/- 0.9 mm (50% of the baseline probing depth) for a total of 317 lesions with a mean baseline depth of 5.4 +/- 0.8 mm. Improvements in clinical parameters achieved with EMD were statistically significant in reference to preoperative measurements. However, despite the overall efficacy of EGR therapy, a significant variation in clinical outcomes was observed. Similar therapeutic results were reported in studies where EGR was compared directly to guided tissue regeneration. However, the controlled clinical trials did not have adequate statistical power to firmly support superiority or equivalency between the 2 regenerative therapies. The statistical superiority of EGR over treatment with open flap debridement has been established. Preliminary histologic investigations with surgically created defects and experimental periodontal lesions demonstrated the ability of EGR to induce formation of acellular cementum and promote significant anaplasis of the supporting periodontal tissues. The potential of EMD to encourage periodontal regeneration was also confirmed in human intrabony defects. However, recent human histologic studies have questioned both the consistency of the histologic outcomes and the ability of EGR to predictably stimulate formation of acellular cementum. Identifying clinical modifying parameters and understanding cellular interactions are apparently essential for the development of methodologies to enhance predictability and extent of EGR clinical and histologic results.
ENDOTOXIN FROM ORAL BACTERIA may be involved in the etiology of the gingival inflammatory lesion. This hypothesis has gained significant support from two re cent articles 2 which have dealt with the role of endo toxin in periodontal disease. Besides presenting a ra tionale for studying endotoxin as a factor involved in the etiology of gingival inflammation, a technique was reported for studying endotoxin in the form in which it might affect the tissues (soluble and in gingival exu date). The method developed was a reproducible, quan titative technique for determining the amount of endo toxin in human gingival exudate. Employing this technique an attempt was made to relate it to the clin ical aspects of the gingival inflammatory lesion. The findings indicated that there was a statistically significant correlation between the quantity of recoverable endo toxin and the clinical degree of inflammation that ex ceeded the 1% level of confidence.The clinical manifestations of gingival inflammation are really a gross expression of the microscopic changes that have taken place in the underlying tissues. There fore, if endotoxin is significantly related to the clinical degree of inflammation, it should also be related to the histologic degree of inflammation in the gingival tissues. It is the subject of this investigation to study whether a correlation exists between the quantity of endotoxin and the histologic degree of inflammation.
FIGURE 1. Section from the center of biopsy specimen (bi opsy N, patient WW). Original magnification lowpower.
MATERIALS AND METHODS
Establishing a Numerical Ranking of the Histologic Degree of InflammationGingival biopsies were taken from 15 patients imme diately after the clinical degree of inflammation had been noted and gingival exudate samples had been pro cured. Since exudate samples were usually obtained from more than one area of the mouth, biopsies were taken of tissue clinically representative of all the areas sampled. The biopsies were processed for histologic ex amination according to accepted methodology, and were then stained with hematoxylin and eosin.A section from the center of each biopsy specimen (Fig. 1) was placed on the stage of a Bausch and Lomb microprojector and was projected onto a piece of white 8X11 inch paper. Tracings were made of the 15 pro jected sections (Fig. 2). Included in each tracing were the outline of the epithelium and the locations of the inflammatory infiltrate. The tracings were laid out on a table and compared as to the histologic degree of in flammation, as determined by the severity and distribu tion of the inflammatory cell infiltrate.
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