Compression Induced Cell Damage in Engineered Muscle Tissue: An In Vitro Model to Study Pressure Ulcer Aetiology

AbstractThe aetiology of pressure ulcers is poorly understood. The complexity of the problem, involving mechanical, biochemical, and physiological factors demands the need for simpler model systems that can be used to investigate the relative contribution of these factors, while controlling others. Therefore, an in vitro model system of engineered skeletal muscle tissue constructs was developed. With this model system, the relationship between compressive tissue straining and cell damage initiation was investigated under well-defined environmental conditions. Compression of the engineered muscle tissue constructs revealed that cell death occurs within 1–2 h at clinically relevant straining percentages and that higher strains led to earlier damage initiation. In addition, the uniform distribution of dead cells throughout the constructs suggested that sustained deformation of the cells was the principle cause of cell death. Therefore, it is hypothetised that sustained cell deformation is an additional mechanism that plays a role in the development of pressure ulcers. © 2003 Biomedical Engineering Society. PAC2003: 8719Rr, 8719Ff, 8718La, 8780Rb

[1]  K. Berecek,et al.  Etiology of decubitus ulcers. , 1975, The Nursing clinics of North America.

[2]  Keith J. Leland,et al.  Temperature-modulated pressure ulcers: a porcine model. , 1995, Archives of physical medicine and rehabilitation.

[3]  Cwj Cees Oomens,et al.  Quantification and localisation of damage in rat muscles after controlled loading; a new approach to study the aetiology of pressure sores. , 2001, Medical engineering & physics.

[4]  R J Errington,et al.  Four-dimensional imaging of living chondrocytes in cartilage using confocal microscopy: a pragmatic approach. , 1997, The American journal of physiology.

[5]  Melissa L. Knothe Tate,et al.  Interstitial Fluid Flow , 2001 .

[6]  T. Husain,et al.  An experimental study of some pressure effects on tissues, with reference to the bed-sore problem. , 1953, The Journal of pathology and bacteriology.

[7]  Erik Buskens,et al.  Prospective cohort study of routine use of risk assessment scales for prediction of pressure ulcers , 2002, BMJ : British Medical Journal.

[8]  Cees W J Oomens,et al.  Monitoring local cell viability in engineered tissues: a fast, quantitative, and nondestructive approach. , 2003, Tissue engineering.

[9]  C. Michel,et al.  Microvascular Mechanisms in Stasis and Ischaemia , 1990 .

[10]  R. Daniel,et al.  Etiologic factors in pressure sores: an experimental model. , 1981, Archives of physical medicine and rehabilitation.

[11]  J G Thacker,et al.  Three-dimensional computer model of the human buttocks, in vivo. , 1994, Journal of rehabilitation research and development.

[12]  S M Dinsdale,et al.  Decubitus ulcers: role of pressure and friction in causation. , 1974, Archives of Physical Medicine and Rehabilitation.

[13]  D. R. Gross,et al.  Three-dimensional tissue deformation in subcutaneous tissues overlying bony prominences may help to explain external load transfer to the interstitium. , 1991, Journal of biomechanics.

[14]  G V Cochran,et al.  Interstitial fluid flow as a factor in decubitus ulcer formation. , 1981, Journal of biomechanics.

[15]  F Guilak,et al.  Volume and surface area measurement of viable chondrocytes in situ using geometric modelling of serial confocal sections , 1994, Journal of microscopy.

[16]  J Bridel,et al.  The aetiology of pressure sores. , 1993, Journal of wound care.

[17]  L M Vistnes,et al.  Differential Response of Skin and Muscle in the Experimental Production of Pressure Sores , 1980, Plastic and reconstructive surgery.

[18]  H. Vandenburgh,et al.  Mechanical stimulation improves tissue-engineered human skeletal muscle. , 2002, American journal of physiology. Cell physiology.

[19]  V. C. Roberts,et al.  The Reaction of Skin and Soft Tissue to Shear Forces Applied Externally to the Skin Surface , 1994 .

[20]  N. P. Reddy.  Effects of Mechanical Stresses on Lymph and Interstitial Fluid Flows , 1990 .

[21]  Cwj Cees Oomens,et al.  The aetiology of pressure sores : a tissue and cell mechanics approach , 1999 .

[22]  H. Vandenburgh,et al.  A simplified method for tissue engineering skeletal muscle organoids in vitro , 1997, In Vitro Cellular & Developmental Biology - Animal.

[23]  Mark D. Fricker,et al.  Aberration control in quantitative imaging of botanical specimens by multidimensional fluorescence microscopy , 1996 .

[24]  Cees W J Oomens,et al.  In vitro models to study compressive strain-induced muscle cell damage. , 2003, Biorheology.

[25]  D. A. Lee,et al.  Compressive Deformation and Damage of Muscle Cell Subpopulations in a Model System , 2001, Annals of Biomedical Engineering.

[26]  J. B. Reswick,et al.  Experience at Rancho Los Amigos Hospital With Devices and Techniques to Prevent Pressure Sores , 1976 .

[27]  Cees W J Oomens,et al.  Predicting local cell deformations in engineered tissue constructs: a multilevel finite element approach. , 2002, Journal of biomechanical engineering.

[28]  J. Faulkner,et al.  Functional development of engineered skeletal muscle from adult and neonatal rats. , 2001, Tissue engineering.

[29]  R Schosser,et al.  Histopathology of pressure ulcers as a result of sequential computer-controlled pressure sessions in a fuzzy rat model. , 1994, Advances in wound care : the journal for prevention and healing.

[30]  H. Vandenburgh,et al.  Tissue-engineered skeletal muscle organoids for reversible gene therapy. , 1996, Human gene therapy.

[31]  E Bell,et al.  Production of a tissue-like structure by contraction of collagen lattices by human fibroblasts of different proliferative potential in vitro. , 1979, Proceedings of the National Academy of Sciences of the United States of America.