Background. Oral mucositis is a common complication of bone marrow transplantation (BMT) conditioning therapy. Sequelae consist of increased risk for infection, moderate to severe pain, compromised oral function, and bleeding. This study investigated helium‐neon laser treatment for prevention of conditioning‐induced oral mucositis in BMT patients. Patterns and severity of mucositis for specific conditioning drug regimens also were analyzed. Methods. Twenty patients received laser radiation to their oral mucosa, either left or right of midline. The contralateral side was sham‐treated and served as a control. Mucositis severity was scored independently by two modified versions of the Oral Mucositis Index Scale (OMI‐A and OMI‐B) and the Eastern Cooperative Oncology Group (ECOG) Oral Toxicity Scale; pain severity was scored by subjects on a visual analogue scale (VAS). Cumulative scores were analyzed for differences between the laser‐treated and sham‐treated sides. Results. Oral mucositis and pain scores were significantly lower for the treated versus the untreated side by OMI‐A and B (P < 0.005) and VAS (P = 0.027) criteria, respectively. Ulcerative lesions occurred in all patients bilaterally; severity increased until Day +6, and lesions resolved by Day +21. Mucositis was more severe for patients conditioned with busulfan/carboplatin/thiotepa than for patients conditioned with busulfan/cyclophosphamide/etoposide. Conclusions. Helium‐neon laser treatment was well‐tolerated and reduced the severity of conditioning‐induced oral mucositis in BMT patients.
Using a specially constructed microscope and transilluminating the intact free gingiva of ferrets, opossums, cats, dogs and rhesus monkeys, blood flow and vascular morphology were observed. Recordings were made on motion picture film at speeds up to 300 frames per second. The state of health of the gingiva was assessed clinically, histologically and by vital microscopy and the three assessments compared. The results indicate that free gingiva which have never been involved in inflammation exhibit a vascular morphology which can be described as a network. With the onset of histopathologic inflammatory changes, the network transforms to a characteristic loop appearance. Five stages of morphologic change are described, based upon the vascular topography seen at various stages of the cellular inflam‐ matory response. It is concluded that the vascular changes of inflammation in the free gingiva of the species studied, precede clinical and epithelial changes.
Vascular perfusion, vital microscopy and conventional histologic techniques were applied to a study of the structure and organisation of vessels in gingiva with no previous history of inflammation. The gingival vasculature around deciduous teeth of cats and dogs was found to be classifiable as a microvascular bed, containing arterioles, precapillary venules and venules less than 50«m in width. Capillaries predominated within crestal gingiva and within the superficial buccal and crevicular networks. Precapillary arterioles and postcapillary venules were most common in the mid gingival region. Small arterioles and venules were present in apical gingiva.Capillaries, comprising the network in crestal gingiva, were arranged as interconnecting repetitive units. Changes in the width, length and local morphology of vessels in each unit, with inflammation, resulted in the formation of vessel loops. With continuing inflammation, certain connecting vessels were lost while other vessels became spatially rearranged.
In order to determine the role of gingival inflammation in the pathogenesis of the gingival enlargment seen in individuals taking diphenylhydantoin sodium (DPH), thirteen female and ten male adult mongrel cats were subjected to a coarse diet, irritating plastic bands around selected teeth, and a daily tooth brushing routine. Fourteen days after initiating the diet, bands, and brushing, 12 of the cats were randomly selected to receive a daily intramuscular injection, 10 mg/kg body weight, of DPH. The remaining cats received the equivalent amount of inert solvent. The maxillary quadrants containing banded teeth were not brushed whilst the maxillary quadrants containing no banded teeth were brushed daily. This combination produced grossly inflamed (banded) and non‐inflamed (non‐banded) maxillary quadrants in two groups of animals; one group receiving DPH, the other receiving vehicle only. The mandibular gingiva were not used in this study. It was possible to reproduce the clinical and histological appearance of DPH gingival enlargement in 11 of the 12 cats receiving DPH and whose gingiva were subjected to local irritation and no oral hygiene. Animals receiving DPH and oral hygiene care, but with no bands on adjacent teeth and thus no local irritation, showed no overt gingival enlargement. Analysis of the results reveals that in the presence of local irritants, producing inflammation, gingival enlargement develops after DPH administration. In the absence of irritants no enlargement occurs.
Ligature‐induced periodontitis was evaluated microbiologically in 8 beagle dogs. Gingival health was established by repeated cleaning. At day 0 subgingival plaque was sampled from individual sites in two quadrants. All teeth in one quadrant were then ligated at the CEJ, and the other quadrant served as a non‐ligated control which was cleaned three times each week. At day 14, four dogs were given metronidazole for seven days. Plaque was cultured anaerobically on nonselcctive media, and the predominant cultivable flora was characterized. At day 0 Gram‐negative facultative rods represented 56.8 % of the flora. with motile and surface translocating organisms predominating. At day 14 Bacteroides asaccharolyticus, including catalase positive B.asaccharolyticus‐like organisms, increased at ligated sites to 34.7 % of the cultivable flora. After metronidazole therapy the total bacterial count decreased, and Gram‐negative anaerobic rods became non‐detectable. Gram negative facultative bacteria which were motile or surface translocating represented 52.7 % of the cultivable flora after metronidazole treatment. In the beagle dog ligature placement was associated with a shift in the flora from Gram‐negative facultative rods to Gram‐negative anaerobic rods. Metronidazole treatment reduced the total cultivable flora and selectively reversed the microflora shifts which followed ligature placement.
The bone resorbing activity of suspensions or supernatants of freeze-dried powdered gingiva was studied by measuring the release of 45Ca from prelabeled fetal rat long bones in organ culture. Two preparations of noninflamed attached gingiva showed no bone resorbing activity, whereas all six preparations of inflamed marginal gingiva tested showed a dose-related stimulation of 45Ca release. Evidence of an osteoclastic mechanism was provided by the inhibition of the bone resorbing activity by calcitonin and cortisol and the minimal activity observed on dead bones. The activity was heat stable and not blocked by human serum. Three different prostaglandin synthetase inhibitors did not inhibit the activity. Immunoassay showed that PGE was present in gingival powder preparations at concentrations in the range 229-2438 pg/mg dry weight. This was insufficient to account for the observed bone resorbing activity by a factor of 50-350. It was concluded that in addition to PGE, inflamed gingiva contains other heat-stable bone resorbing factor(s).
Measurements of erythrocyte velocity in vascular networks of noninflamed gingiva of deciduous canines of four young dogs were obtained using vital microscopy and high-speed cinephotomicrography. Mean erythrocyte velocity in small gingival vessels was 1.59 +/- 0.29 mm/sec. Differences in erythrocyte velocity of vessels comprising a gingival microcirculation and of vessels within different gingival samples were not significant.
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