S C Marks1. 1. Department of Otolaryngology, Wayne State University School of Medicine, Detroit, Michigan, USA.
Abstract
OBJECTIVES: Characterize the histology of the rhinogenic model of sinusitis and compare this with existing models of sinusitis. STUDY DESIGN: Prospective controlled trial in animals. METHODS: New Zealand white rabbits were implanted with a synthetic sponge, which was then impregnated with Streptococcus pneumoniae bacteria. After a specified time the animals were sacrificed, and whole-mount sectioning of both the infected and noninfected sinuses was performed. The sinuses were carefully examined for evidence of inflammatory changes. RESULTS: This model produced a sinus infection that is characterized by luminal exudates of neutrophils and eosinophils, mucosal infiltration with lymphocytes and plasma cells, and epithelial degeneration. In addition, discrete lymphoid follicles were identified in both the implanted and nonimplanted sides that in the implanted sides appear to hypertrophy and liberate leukocytes into the sinus lumen. Other areas were observed where luminal exudates seem to act on and degrade mucosa that has little or no underlying inflammation. In severely infected sinuses submucosal vacuole formation with overlying granulation tissue was observed. CONCLUSIONS: The rhinogenic model of sinusitis demonstrates features typical of other known models of sinusitis. In addition, there appear to be unique features of this model, specifically the identification of discrete lymphoid aggregates, which suggest that this model has the potential to be valuable for the study of the immune response of the sinuses.
OBJECTIVES: Characterize the histology of the rhinogenic model of sinusitis and compare this with existing models of sinusitis. STUDY DESIGN: Prospective controlled trial in animals. METHODS: New Zealand white rabbits were implanted with a synthetic sponge, which was then impregnated with Streptococcus pneumoniae bacteria. After a specified time the animals were sacrificed, and whole-mount sectioning of both the infected and noninfected sinuses was performed. The sinuses were carefully examined for evidence of inflammatory changes. RESULTS: This model produced a sinus infection that is characterized by luminal exudates of neutrophils and eosinophils, mucosal infiltration with lymphocytes and plasma cells, and epithelial degeneration. In addition, discrete lymphoid follicles were identified in both the implanted and nonimplanted sides that in the implanted sides appear to hypertrophy and liberate leukocytes into the sinus lumen. Other areas were observed where luminal exudates seem to act on and degrade mucosa that has little or no underlying inflammation. In severely infected sinuses submucosal vacuole formation with overlying granulation tissue was observed. CONCLUSIONS: The rhinogenic model of sinusitis demonstrates features typical of other known models of sinusitis. In addition, there appear to be unique features of this model, specifically the identification of discrete lymphoid aggregates, which suggest that this model has the potential to be valuable for the study of the immune response of the sinuses.
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