Biomedical subjects

A E Tami

Publications and source records attributed to A E Tami.

3 recordsLinked to original sources

PubMed2003

Noninvasive fatigue fracture model of the rat ulna.

Fatigue damage occurs in response to repeated cyclic loading and has been observed in situ in cortical bone of humans and other animals. When microcracks accumulate and coalesce, failure ensues and is referred to as fatigue fracture. Experimental study of fatigue fracture healing is inherently difficult due to the lack of noninvasive models. In this study, we hypothesized that repeated cyclic loading of the rat ulna results in a fatigue fracture. The aim of the study was to develop a noninvasive long bone fatigue fracture model that induces failure through accumulation and coalescence of microdamage and replicates the morphology of a clinical fracture. Using modified end-load bending, right ulnae of adult Sprague-Dawley rats were cyclically loaded in vivo to fatigue failure based on increased bone compliance, which reflects changes in bone stiffness due to microdamage. Preterminal tracer studies with 0.8% Procion Red solution were conducted according to protocols described previously to evaluate perfusion of the vasculature as well as the lacunocanalicular system at different time points during healing. Eighteen of the 20 animals loaded sustained a fatigue fracture of the medial ulna, i.e. through the compressive cortex. In all cases, the fracture was closed and non-displaced. No disruption to the periosteum or intramedullary vasculature was observed. The loading regime did not produce soft tissue trauma; in addition, no haematoma was observed in association with application of load. Healing proceeded via proliferative woven bone formation, followed by consolidation within 42 days postfracture. In sum, a noninvasive long bone fatigue fracture model was developed that lends itself for the study of internal remodeling of periosteal woven bone during fracture healing and has obvious applications for the study of fatigue fracture etiology.

Animals↗

PubMed2003

Probing the tissue to subcellular level structure underlying bone's molecular sieving function.

Transport of fluorescent probes between 300 and 2,000,000 Da was studied in mechanically loaded and unloaded ulnae of skeletally mature rats to characterize the permeability of the pericellular space of the lacunocanalicular system (LCS), and the microporosity of the bony matrix. The mineral matrix porosity allowed for penetration of the 300 Da probe but impeded transport of larger probes. The pericellular space of the LCS was permeable up to 10 kDa; above 10 kDa, diffusion was ineffective for transport through the pericellular space. Convective transport via load-induced fluid flow increased penetration of all probes up to 70 kDa. Above this threshold, probes were excluded from bone, both with and without loading. This exploratory study suggests that bone acts as a molecular sieve and that mechanical loading modulates transport of solutes through the pericellular space that links osteocytes deep within the tissue to the blood supply and to osteoblasts and osteoclasts on bone forming and resorbing surfaces. This provides support for the postulate of transport modulated bone remodeling in which osteocytes are influenced by and modulate the local permeability of their surroundings as a means for survival (Knothe Tate et al. 1998, [28]) and has profound implications for osteocyte viability and intercellular communication in bone.

Animals↗

PubMed2002

The role of interstitial fluid flow in the remodeling response to fatigue loading.

Load-induced fluid flow enhances molecular transport through bone tissue and relates to areas of bone resorption and apposition. Remodeling activity is highly coordinated and necessitates a means for cellular communication via intracellular and extracellular means. Osteocytes, osteoblasts, and osteoclasts, which reside in disparate locations within the tissue, communicate intracellularly via the cellular syncytium and extracellularly via the pericellular fluid space of the lacunocanalicular system. Both of these communications systems are physically disrupted by microdamage incurred during fatigue loading of bone. The purpose of this study was to develop an analytical model to understand the role of interstitial fluid flow in the remodeling response to fatigue loading. Adequate transport was assumed a prerequisite for maintenance of cell viability in bone. Diffusive and convective transport were simulated through the lacunocanalicular network in a healthy undamaged state as well as in a damaged state after fatigue loading. The model predicts that fatigue damage impedes transport from the blood supply, depleting the concentration of molecular entities in and downstream from areas of damage. Furthermore, the presence of microcracks alters the distribution of molecular entities between individual lacunae. These effects were confirmed by the results of an in vivo pilot study in which fluorescent, flow-visualizing agents pooled within microcracks and were absent from areas surrounding microcracks, corresponding to areas deprived of fluid flow. Loss of osteocyte viability is coupled to targeting and initiation of new remodeling activity. Taken as a whole, these data suggest a link between interstitial fluid flow, mass transport, maintenance of osteocyte viability, and modulation of remodeling activity.

Biological Transport↗