Articular cartilage is subjected to dynamic compressive loading that is known to influence chondrocyte metabolism. While the exact signalling mechanisms are unclear, it has been proposed that cell deformation plays a role and may stimulate a metabolic response through distinctive pathways. In this study, a well characterized model system in which chondrocytes are embedded in agarose was used to study the effect of dynamic cellular strain on three key metabolic processes, namely the synthesis of glycosaminoglycan, of DNA, and of total protein. Using a specially designed apparatus, 15% compressive strain amplitude was applied to agarose-chondrocyte cylinders statically or dynamically over a range of frequencies (0.3-3 Hz). Static and low-frequency strain (0.3 Hz) inhibited the synthesis of glycosaminoglycan, while a frequency of 1 Hz stimulated synthesis. Static strain reduced the level of thymidine uptake, whereas dynamic strain at all frequencies induced an increase in chondrocyte proliferation. Incorporation of tritiated proline was suppressed by all strain regimens tested. The three parameters investigated were each influenced by the dynamic strain regimens in a distinct manner, implying that the signalling mechanisms involved are uncoupled.

AimThis paper discusses the critical determinants of pressure ulcer development and proposes a new pressure ulcer conceptual framework.BackgroundRecent work to develop and validate a new evidence-based pressure ulcer risk assessment framework was undertaken. This formed part of a Pressure UlceR Programme Of reSEarch (RP-PG-0407-10056), funded by the National Institute for Health Research. The foundation for the risk assessment component incorporated a systematic review and a consensus study that highlighted the need to propose a new conceptual framework.DesignDiscussion Paper.Data SourcesThe new conceptual framework links evidence from biomechanical, physiological and epidemiological evidence, through use of data from a systematic review (search conducted March 2010), a consensus study (conducted December 2010–2011) and an international expert group meeting (conducted December 2011).Implications for NursingA new pressure ulcer conceptual framework incorporating key physiological and biomechanical components and their impact on internal strains, stresses and damage thresholds is proposed. Direct and key indirect causal factors suggested in a theoretical causal pathway are mapped to the physiological and biomechanical components of the framework. The new proposed conceptual framework provides the basis for understanding the critical determinants of pressure ulcer development and has the potential to influence risk assessment guidance and practice. It could also be used to underpin future research to explore the role of individual risk factors conceptually and operationally.ConclusionBy integrating existing knowledge from epidemiological, physiological and biomechanical evidence, a theoretical causal pathway and new conceptual framework are proposed with potential implications for practice and research.

During physiological loading, a tendon is subjected to tensile strains in the region of up to 6 per cent. These strains are reportedly transmitted to cells, potentially initiating specific mechanotransduction pathways. The present study examines the local strain fields within tendon fascicles subjected to tensile strain in order to determine the mechanisms responsible for fascicle extension. A hierarchical approach to the analysis was adopted, involving micro and macro examination. Micro examination was carried out using a custom-designed rig, to enable the analysis of local tissue strains in isolated fascicles, using the cell nuclei as strain markers. In macro examination, a video camera was used to record images of the fascicles during mechanical testing, highlighting the point of crimp straightening and macro failure. Results revealed that local tensile strains within a collagen fibre were consistently smaller than the applied strain and showed no further increase once fibres were aligned. By contrast, between-group displacements, a measure of fibre sliding, continued to increase beyond crimp straightening, reaching a mean value of 3.9 per cent of the applied displacement at 8 per cent strain. Macro analysis displayed crimp straightening at a mean load of 1 N and sample failure occurred through the slow unravelling of the collagen fibres. Fibre sliding appears to provide the major mechanism enabling tendon fascicle extension within the rat-tail tendon. This process will necessarily affect local and cellular strains and consequently mechanotransduction pathways.

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