Background Total wrist replacement (TWR) as motion-preserving procedure continues to be critically discussed in the literature, although the complication rates have been significantly reduced with the current 3rd generation designs compared with older types. Possible reasons for this are often also a lack of knowledge about the currently available evidence, the complication management, and the lack of practical experience by the surgeons. Methods Based on an extended review of literature and own experience, the aim of this article is to give practicable insights for the clinician on: (1) biomechanical fundamentals, (2) differences in design, survivorship and functional outcome between the recent types, (3) possible pitfalls, and (4) failures and salvage options. Results The goal of TWR is that the overall wrist motion is maintained respectively improved despite it works with a locked midcarpal joint. Regarding survivorship and functional outcome the Maestro is (was) being superior over all other types that is (was) based on features in design. There is no scientific evidence as to why the Maestro was withdrawn from the marketplace by the company. For assessment of instability and/or impingement the use of dynamic radiographs is recommended. The problem of TWR is unchanged failure of the carpal components primarily based on mechanical dysbalance, and secondarily followed by metal and/or polyethylene wear, but surgical revision of asyptomatic periprosthetic osteolysis without safe radiagraphic signs of loosening is only required in not more than 20% of cases. For a failed TWR, revision TWR or conversion to total wrist arthrodesis are viable salvage options. Conclusions The knowledge about recent evidence and features in design of the available types, exact assessment of radiographic findings, presence of technical skills by the surgeons, and observance of the patient's expectations are the basic requirements for a successful TWR.
The effects of GH and PTH on cancellous histomorphometry were determined in the proximal tibial metaphysis of hypophysectomized (HYPOX) sexually mature female rats. HYPOX resulted in uterine atrophy and a loss in body weight. Longitudinal bone growth ceased and bone formation was greatly reduced. There were decreases in cancellous bone area, trabecular number, and trabecular thickness. Intermittent treatment with GH did not influence uterine weight in HYPOX rats. However, GH resulted in resumption of whole body weight gain, as well as maintenance of normal longitudinal bone growth. Additionally, GH partially maintained bone formation in HY POX rats and did not have a significant effect on steady state messenger RNA levels for osteocalcin. Intermittent treatment with PTH had no effect on whole body weight gain, uterine weight, or longitudinal bone growth. In contrast, PTH increased bone formation compared with the baseline, HYPOX, and GH-treated HYPOX rats, and dramatically increased osteocalcin messenger RNA levels compared with the latter two groups. The increased bone formation was primarily due to an increase in osteoblast number; the mineral apposition rate, an index of osteoblast activity, was increased compared with control and GH-treated rats but not compared with baseline values. Interestingly, neither treatment influenced indices of bone resorption.
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