Deep tissue injury (DTI), as a recently emphasized mechanism for PU formation [1], has received increased attention lately and several studies reported findings on newly developed DTI animal models [2]. The clinical view of DTI emphasizes the severity of clinically identified DTI as that a true DTI progresses rapidly even with the most aggressive treatment and its massive tissue necrosis is in a similar nature of a Stage-IV full-thickness wound [3]. Many animal PU models have been developed to test different hypotheses related to deep tissue injury (DTI) [3]. However, none of DTI studies reported that the experimentally induced DTI eventually progressed to be an open wound which affected superficial skin, and the reported histological or imaging data of the induced DTI did not suggest massive tissue necrosis. Although it might be that most studies did not keep their DTI animals long enough to observe the formation of an open wound from the DTI, the results from our own observation and Kwan, et al [4], in which no skin lesion was formed after 7 days of DTI, do not support this speculation. It may be that, in these DTI studies, the injured deep layer had healed. By examination of the existing PU rat models, especially those for DTI research, we came to our assumption that the missing bony prominence may possibly be a flaw that prevents those models from yielding more clinically relevant data. It has long been the understanding that PUs often occur at tissue pressure points around a bony prominence. We believe that, to more accurately simulate the clinical scenario of DTI formation, a bony prominence is necessary for a rat DTI model.

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