Publications

1983

Donohue, J M, D Buss, T R Oegema, and R C Thompson. (1983) 1983. “The Effects of Indirect Blunt Trauma on Adult Canine Articular Cartilage.”. The Journal of Bone and Joint Surgery. American Volume 65 (7): 948-57.

UNLABELLED: In order to determine the effect of subfracture loads on articular cartilage, we impacted twelve adult canine patellofemoral joints utilizing a drop-tower with two different force-levels. The joints were examined with light and electron microscopy at two, four, and six weeks after impaction. In ten additional animals a single knee was impacted and they were analyzed biochemically at similar time-periods, using the contralateral joint as a control. In all impacted specimens changes were observed in the zone of calcified cartilage, represented by an increase in cellular clones, vascular invasion, and proteoglycan content of the matrix. Ultrastructural evaluation of the superficial and deep radial zones of the articular cartilage revealed loss of the cellular processes and territorial matrices of chondrocytes in both layers. Ruthenium-red staining of impacted samples revealed a 40 per cent decrease in proteoglycan associated with collagen fibers in the extraterritorial matrix. An increase in collagen-fiber width was observed in the four and six-week groups. The earliest changes in articular cartilage included activation of the zone of calcified cartilage as well as ultrastructural alterations in the superficial and radial zones. Biochemical analysis revealed an increase in water content and hexuronic acid at two weeks. These changes occurred at a subfracture level in the absence of surface disruption.

CLINICAL RELEVANCE: These animal experiments indicate that adult articular cartilage may show significant alterations in its histological, biochemical, and ultrastructural characteristics without disruption of the articular surface. This model of articular cartilage "contusion" may represent a corollary to the joint damage that is observed following direct blunt trauma transmitted across articular surfaces without radiographic evidence of fracture. The possibility that this form of injury may be the precursor of chondromalacic changes in patellar or femoral cartilage merits further study.

1979

Choudhury, S R, N A Azzam, and J M Donohue. (1979) 1979. “Changes in the Surface Fine Structure of Rat Third Ventricular Ependyma Following Chronic Acetazolamide Treatment.”. Journal of Anatomy 129 (Pt 1): 51-62.

Participation of non-choroidal elements, particularly of ventricular ependyma, in CSF production is well recognized. The present investigation is an attempt to elucidate possible surface changes in the ventricular lining following chronic acetazolamide administration in the rat. A progressive time-dependent change was observed in the ependyma of the third ventricle. In the dorsal ciliated zone the appearance of dilatations and surface evaginations on cilial shafts were the predominent features. The ventral non-cilated area was characterized by eruption of blebs and microvilli with apical swellings. The significance of these surface fine structural changes are discussed in the light of available studies. It appears that the ependyma is stimulated into increased activity. However, the precise nature of such a response–whether secretory or absorptive–must remain conjectural until correlative scanning and transmission electron microscopic data become available.

1978

Azzam, N A, S R Choudhury, and J M Donohue. (1978) 1978. “Changes in the Surface of Fine Structure of Choroid Plexus Epithelium Following Chronic Acetazolamide Treatment.”. Journal of Anatomy 127 (Pt 2): 333-42.

Surface changes in the epithelium of the choroid plexuses of the lateral and third ventricles of rats induced by chronic administration of acetazolamide have been studied by scanning electron microscopy. After 3 weeks atrophic changes were evident, the microvilli and blebs normally seen on the ventricular surface of the cells appeared attenuated, and in extreme cases they disappeared, leaving the cell surface completely denuded. Localized areas of hypertrophy, indicated by secondary spherical budding, were occasionally observed. The atrophic changes accord with the known inhibitory effects of acetazolamide on CSF formation: perhaps the small number of cells undergoing hypertrophy compensate to some extent for the atrophic ones and maintain some CSF secretion.

1948