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Biomedical subjects

B Loitz-Ramage

Publications and source records attributed to B Loitz-Ramage.

3 recordsLinked to original sources

Measuring knee joint laxity: a review of applicable models and the need for new approaches to minimize variability.

Knee joint laxity can result from soft tissue injury, such as a ligament tear, or from genetic factors such as joint hypermobility syndrome and various forms of Ehlers-Danlos Syndrome. The location of a subject's passive knee laxity along a continuous spectrum is dependent on the mechanical properties of the existing structures, and the increased motion that often follows joint injury. At a threshold along the spectrum, a patient will be at risk for joint instability and further injury to joint structures. Links between instability and laxity may be better understood if laxity can be reliably and accurately quantified. Current measures of laxity have not been compared to a 'gold standard' in all cases, and when they have, were found to overestimate the laxity values. This is attributed to soft tissue deformation. Consequently, a noninvasive measure of laxity with improved accuracy and repeatability would be useful clinically and in the research sector. In this review, current clinical measures of laxity are critiqued, criteria for a measure of laxity are identified, and three theoretical models of knee laxity are outlined. These include contact, lumped parameter, and finite element models, with emphasis on applicability, strengths, and limitations of each. The long term goal is to develop a model and method able to differentiate subjects along a spectrum of laxity, and understand the functional implications of altered joint integrity. This would allow careful scrutiny of clinical interventions aimed at improving joint health and provide a valuable research tool to study joint injury, healing, and degeneration.

Anterior Cruciate Ligament↗

A structurally based stress-stretch relationship for tendon and ligament.

We propose a mechanical model for tendon or ligament stress-stretch behavior that includes both microstructural and tissue level aspects of the structural hierarchy in its formulation. At the microstructural scale, a constitutive law for collagen fibers is derived based on a strain-energy formulation. The three-dimensional orientation and deformation of the collagen fibrils that aggregate to form fibers are taken into consideration. Fibril orientation is represented by a probability distribution function that is axisymmetric with respect to the fiber. Fiber deformation is assumed to be incompressible and axisymmetric. The matrix is assumed to contribute to stress only through a constant hydrostatic pressure term. At the tissue level, an average stress versus stretch relation is computed by assuming a statistical distribution for fiber straightening during tissue loading. Fiber straightening stretch is assumed to be distributed according to a Weibull probability distribution function. The resulting comprehensive stress-stretch law includes seven parameters, which represent structural and microstructural organization, fibril elasticity, as well as a failure criterion. The failure criterion is stretch based. It is applied at the fibril level for disorganized tissues but can be applied more simply at a fiber level for well-organized tissues with effectively parallel fibrils. The influence of these seven parameters on tissue stress-stretch response is discussed and a simplified form of the model is shown to characterize the nonlinear experimentally determined response of healing medial collateral ligaments. In addition, microstructural fibril organizational data (Frank et al., 1991, 1992) are used to demonstrate how fibril organization affects material stiffness according to the formulation. A simplified form, assuming a linearly elastic fiber stress versus stretch relationship, is shown to be useful for quantifying experimentally determined nonlinear toe-in and failure behavior of tendons and ligaments. We believe this ligament and tendon stress-stretch law can be useful in the elucidation of the complex relationships between collagen structure, fibril elasticity, and mechanical response.

Animals↗

Hyperbaric oxygen in the treatment of acute muscle stretch injuries. Results in an animal model.

Hyperbaric oxygen therapy is an established therapy in several areas of clinical medicine. However, studies have produced conflicting results regarding its efficacy for sports-related soft tissue injuries. This study examines the use of hyperbaric oxygen therapy after an acute muscle stretch injury in an animal model. Two groups of rabbits (nine in each group) were subjected to a partial stretch injury to the tibialis anterior muscle-tendon unit. For all 18 animals, the injuries were induced in the left limb, and the uninjured right limb served as a sham-operated control. In group 1, the animals were exposed to hyperbaric oxygen (> 95% O2 at 2.5 atm) for 60 minutes daily for 5 days. Treatment began 24 hours after injury. Group 2 animals were not exposed to hyperbaric oxygen. Evaluation 7 days after injury demonstrated a functional deficit (percent ankle isometric torque; injured side versus uninjured side) of 14.9% +/- 5.5% (mean +/- SD) for the treated group and 47.5% +/- 5.4% for the untreated group, representing a statistical difference using the Behrens-Fisher version of the t test (P = 0.001). Morphologic studies revealed more complete healing in the treated group. This study suggests that hyperbaric oxygen therapy may play a role in accelerating recovery after acute muscle stretch injury. Further studies are needed before definitive conclusions and treatment recommendations can be made.

Animals↗