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Tissue Proliferation (tissue + proliferation)
Selected AbstractsEvaluation of the chondral modeling theory using fe-simulation and numeric shape optimizationJOURNAL OF ANATOMY, Issue 5 2009Jeffrey H. Plochocki Abstract The chondral modeling theory proposes that hydrostatic pressure within articular cartilage regulates joint size, shape, and congruence through regional variations in rates of tissue proliferation. The purpose of this study is to develop a computational model using a nonlinear two-dimensional finite element analysis in conjunction with numeric shape optimization to evaluate the chondral modeling theory. The model employed in this analysis is generated from an MR image of the medial portion of the tibiofemoral joint in a subadult male. Stress-regulated morphological changes are simulated until skeletal maturity and evaluated against the chondral modeling theory. The computed results are found to support the chondral modeling theory. The shape-optimized model exhibits increased joint congruence, broader stress distributions in articular cartilage, and a relative decrease in joint diameter. The results for the computational model correspond well with experimental data and provide valuable insights into the mechanical determinants of joint growth. The model also provides a crucial first step toward developing a comprehensive model that can be employed to test the influence of mechanical variables on joint conformation. [source] Clinical Resolution of a Neonatally Eroded Giant Congenital Melanocytic NevusPEDIATRIC DERMATOLOGY, Issue 6 2006Julia K. Gass M.R.C.P.C.H. This process has been documented with photographs and skin biopsy specimens. Neonatal histology demonstrated connective tissue proliferation. Histology at age 5 years also demonstrated a very high proportion of amelanotic dermal nevus cells. Regression of pigmentation in our patient may be due to a decrease in melanin production by dermal nevus cells rather than a decrease in their number. [source] Functional adaptation of the femoral head to voluntary exerciseTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 7 2006Jeffrey H. Plochocki Abstract The functional adaptation of limb joints during postnatal ontogeny is necessary to maintain proper joint function. Joint form is modified primarily through differential rates of articular cartilage proliferation across articular surfaces during endochondral growth. This process is hypothesized to be mechanically regulated by the magnitude and orientation of stresses in the articular cartilage. However, the adaptation of limb joint morphology to the mechanical environment is poorly understood. We investigate the effects of voluntary exercise on femoral head morphology in 7-week-old female mice of the inbred strain C57BL/6J. The mice were divided into a control group and a group treated with voluntary access to an activity wheel for the duration of the 4-week study. Histomorphometric comparisons of chondral and osseous joint tissue of the proximal femur were made between control and exercise treatment groups. We find that exercised mice have significantly thicker articular cartilage with greater chondral tissue area and cellularity. Exercised mice also exhibit significantly greater bone tissue area and longer and flatter subchondral surfaces. No significant difference is found in the curvature of the articular cartilage or the length of the chondral articular surface between groups. These data suggest that a complex mechanistic relationship exists between joint stress and joint form. Joint tissue response to loading is multifaceted, involving both size and shape changes. Our data support the hypothesis that joint growth is ontogenetically plastic. Mechanical loading significantly influences chondral and subchondral tissue proliferation to provide greater support against increased mechanical loading. Anat Rec Part A, 288A:776,781, 2006 © 2006 Wiley-Liss, Inc. [source] T and B lymphocyte depletion has a marked effect on the fibrosis of dystrophic skeletal muscles in the scid/mdx mouse,THE JOURNAL OF PATHOLOGY, Issue 2 2007A Farini Abstract Abnormal connective tissue proliferation following muscle degeneration is a major pathological feature of Duchenne muscular dystrophy (DMD), a genetic myopathy due to lack of the sarcolemmal dystrophin protein. Since this fibrotic proliferation is likely to be a major obstacle to the efficacy of future therapies, research is needed to understand and prevent the fibrotic process in order to develop an effective treatment. Murine muscular dystrophy (mdx) is genetically homologous to DMD, and histopatological alterations are comparable to those of the muscles of patients with DMD. To investigate the development of fibrosis, we bred the mdx mouse with the scid immunodepressed mouse and analysed fibrosis histologically; we used ELISA analysis to determine TGF-,1 expression. Significant reduction of fibrosis and TGF-,1 expression was found in the muscles of the scid/mdx mice. However, we observed similar centrally located nuclei, necrosis, muscle degeneration and muscle force compared to the mdx animals. These data demonstrate a correlation between the absence of B and T lymphocytes and loss of fibrosis accompanied by reduction of TGF-,1, suggesting the importance of modulation of the immune system in DMD. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. [source] | |||||||||||||