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Biomedical subjects

B R Rittman

Publications and source records attributed to B R Rittman.

13 recordsLinked to original sources

Healing of induced periapical lesions in ferret canines.

A previous study showed that the ferret canine is an appropriate model for inducing periapical lesions. Ferret canines were used in this study to study changes in periapical lesions after root canal treatment (RCT). After periapical pathosis was induced in the maxillary and mandibular canines of six ferrets, RCT was performed on three of the four canines in each animal. Each ferret received periodic intraperitoneal injections of Procion red dye. Two animals were killed at each of 4, 8, and 12 wk after RCT. Apices and surrounding lesions were evaluated radiographically, histologically, and by fluorescent microscopy. Periapical radiolucencies increased in size during induction but showed no changes after RCT. Lesions in untreated teeth showed features of granulomatous inflammation, mainly the presence of macrophages and lymphocytes. After RCT, there was histological evidence of healing in the form of cementum deposition, increased vascularity, and increased fibroblastic and osteoblastic activity. Fluorescent staining showed cementum deposition of variable thickness in the treated specimens.

Animals↗

Induced periapical lesions in ferret canines: histologic and radiographic evaluation.

Ferrets have been utilized in endodontic research to study periapical responses. However, various aspects of induction and healing of periapical pathosis in ferrets are unclear. This study evaluated the radiographic and histopathologic features of induced periapical lesions. Periapical pathosis was consistently produced in 8 canines of 2 ferrets by extirpating the pulp, leaving the cavities open for a week, then sealing for 12 weeks. The resulting lesions were evaluated radiographically every two weeks. The animals were then killed and the induced lesions evaluated histologically and histobacteriologically. Four untreated canines from 2 other ferrets were used as controls. Results showed that periapical rarefactions were visible in all teeth in the experimental group within 4 weeks. Histologically, the induced lesions consisted principally of a mononuclear inflammatory infiltrate, dominated by macrophages but with numerous lymphocytes. With Brown & Brenn staining, bacteria were demonstrated in the pulp space of teeth in which the lesions were induced and in the apical arborization of the canal system. Only one specimen had bacteria within the periapical lesion.

Animals↗

Replacement of Langerhans cells in murine palate.

Palates from C3H mice were implanted onto prepared graft beds in histocompatible F1 hybrid mice. Biopsies taken 1, 2, 4, 8, and 16 wk later were prepared to demonstrate Langerhans cells (LC) of C3H and F1 (host) origin. After 1 wk only occasional LC (all of C3H origin) were present. By 2 wk total LC numbers had increased to a level approximately 50% greater than in control (non-implanted) palate, with most of this increase due to C3H LC proliferation. From 4 through 16 wk total LC numbers were not significantly different from those of control palate. During weeks 2 through 16 the percentages of LC of F1 origin were 31, 70, 39, and 19% respectively. These results indicate an increased proliferation of C3H LC with an initial migration of F1 LC which stops as C3H LC numbers increase.

Animals↗

Immunocytochemical examination of immune cells in periapical granulomata and odontogenic cysts.

Monoclonal antibodies (mAbs) were used to determine the presence and distribution of immune cells including lymphocytes, macrophages and Langerhans cells, in normal periodontal ligament, periapical granulomata, periapical cysts and dental developmental cysts. Isolated T-lymphocytes, but not B-lymphocytes, were detected in specimens of non-inflamed periodontal ligament. Increased numbers of T and B lymphocytes were found in all of the lesions examined. Monocytes/macrophages were associated with most periapical granulomata, dental developmental cysts and all periapical cysts. Langerhans cells, intraepithelial lymphocytes, and monocytes/macrophages were not detected in the rests of Malassez but were found in some epithelia within periapical granulomata and in most epithelial linings of odontogenic cysts. Increased numbers of immune cells were seen around proliferative epithelia and adjacent to the epithelial linings of cysts. Epithelium, particularly that of odontogenic cysts, showed positive reactions for HLA-Dr, lysozyme and for alpha-1 antitrypsin. The presence of immune cells in periapical granulomata and odontogenic cysts, suggests that cell-mediated and humoral immunoreactions occur in these lesions and may be associated with the epithelial proliferation within the periapical lesions.

Adult↗

Age-associated changes in Langerhans cells of murine oral epithelium and epidermis.

Oral mucosa and skin of older individuals are immunologically less responsive to a range of allergens, but it is not known whether this is due to changes in the number of Langerhans cells or to impaired cell function. EDTA-separated epithelial sheets from the cheek and palate mucosa, and from ear aN< footpad skin of three-month-old and 24-month-old C57BL/6NNia mice were stained for ATPase, beta-glucuronidase activity and Iab-surface antigen to demonstrate Langerhans cells. The general distribution of such cells was unchanged with age, but those in epithelia from the old mice were more varied in shape, with irregular celL bodies and more elongated dendritic processes. The numerical density of Langerhans cells in old mice was reduced by 30-59 per cent compared with that in young mice.

Aging↗

Effects of histological processing on lectin binding patterns in oral mucosa and skin.

The effects of fixation and wax processing on lectin binding to C3H mouse palate and tail skin were evaluated using eight FITC-conjugated lectins. Sections and blocks of tissue were fixed in acetone, ethanol, methanol, formalin, glutaraldehyde or Bouin's picric-acetic-formalin fixative. Tissue blocks were then processed to paraffin wax. Compared to unfixed cryostat sections, there was a weaker but similar pattern of surface binding to sections of fixed and wax-processed tissues with acetone, alcohols and Bouin's fixative. Basement membrane binding was much weaker with acetone-wax and absent when alcohols or Bouin's fixatives were used. Tissues fixed in formalin showed very weak general binding, while glutaraldehyde fixation resulted in considerable non-specific cytoplasmic binding. Acetone, alcohols or Bouin's fixative followed by processing to paraffin wax provided convenient acceptable alternatives to the use of unfixed cryostat sections. Lipid extraction prior to lectin incubation resulted in complete elimination of detectable binding to epithelium suggesting that lectin-binding sites in the cell surface are associated with glycolipid or lipid.

Acetone↗

Lectin binding to murine oral mucosa and skin.

Carbohydrates on epithelial cell surfaces of oral mucosa and skin from various anatomical regions of C3H mice were demonstrated with fluoresceinated lectins. With an individual lectin, all tissues showed a similar pattern of binding: most lectins showed binding to the cell surfaces of all nucleated cell layers although that to basal cells was often weaker and was occasionally absent. The corneocytes did not typically bind lectins except that the follicular keratin of the tail showed a uniform and intense fluorescence with several lectins. Basement membrane bound all lectins. The results indicate that detectable changes occur in the cell-surface carbohydrate composition as cells differentiate but that cell-surface carbohydrates do not differ markedly from one region to the next. Lectin binding may provide a convenient method of detecting functional changes in normal cells and in cells which have undergone experimental or pathological changes.

Animals↗

Reactivity of epidermal Langerhans cells to a histochemical method for demonstration of beta-glucuronidase.

Sheets or sections of mouse epidermis reacted by a histochemical method for the enzyme beta-glucuronidase display a subpopulation of dendritic cells which correspond in number and spacing to Langerhans cells demonstrated by reactivity for ATPase or Ia antigens. A similar staining pattern is seen in rat, rabbit, and guinea pig epidermis. In rhesus monkey and human skin, Langerhans cells appear to be reactive for beta-glucuronidase but, as keratinocytes are also reactive, Langerhans cells are not readily identifiable by this method. The thermal stability of beta-glucuronidase differs between strains of mice. Langerhans cells of Balb/C and C3H strains can thus be distinguished by appropriate pretreatment before incubation, a method of potential value for experimental investigations of the origin of Langerhans cells.

Adenosine Triphosphatases↗

Quantitative characterization of changes in cellularity and collagen fiber size in contracting palatal wounds.

Standard surgical wounds with either plain or undermined margins were created in the hard palates of 15 beagle pups by excising a strip of mucoperiosteum adjacent to molars. Healing was monitored, the pups were sacrificed at intervals from five to 31 days after surgery. Longitudinal data were collected for body weight and wound contraction. Examination of histologic sections of the wounds and adjacent tissues involved visual light microscopic assessments of fibroblast population density and computerized image analysis microscopy for quantification of population densities of three sizes of collagen fibers. Wounds with undermined margins showed less contraction than did those having plain margins. Findings on changes in the morphologic character of the maturing granulation tissues included quantitative documentation of (a) decreases in the population density of fibroblasts, (b) marked decreases in the number of thin (reticular) fibers, (c) marked increases in the number of medium sized fibers, and (d) slight increases in the number of coarse fibers.

Animals↗

Dentinal crazing and interpin distance.

All three types of self-threading plus cause dentinal crazing. The frequency and degree of damage done to the dentin varies significantly between the three types of pins and depends upon the differences in the diameters of the drill and the pin. When two or more pins are placed in dentin, the potential for dentinal damage increases. Minikin pins (0.019-inch diameter) caused the least damage, in terms of both degree and frequency. The optimum and safe interpin distance using Minikin pins suggested by this study is 3 mm. Minim and Regular pins (0.023- and 0.031-inch diameters, respectively) caused more injury than Minikin pins. The Regular pins showed more damaging effects on dentin than Minim pins, both in terms of degree and frequency. On the basis of this study, the minimum interpin distance using Minim or Regular pins should be 5 mm. These minimum interpin distances are applicable only in situations where the dentin is not dehydrated or embrittled due to endodontic treatment. In teeth that have been endodontically treated, it would be advisable to use only the smallest self-threading pins and possibly increase the interpin distance if two or more pins are to be used.

Dental Pins↗