DOES TOTAL KNEE REPLACEMENT MODIFY THE SERUM LEVEL OF INTACT-PARATHYROID HORMONE IN POSTMENOPAUSAL WOMEN SUFFERING FROM END-STAGE KNEE OSTEOARTHRITIS?

Abstract

Introduction: Parathyroid hormone (PTH) is a major regulator of bone metabolism. Continuously elevated levels of PTH activate osteoclasts, whereas its intermittent administration principally induces osteoblastic activity. There is increasing evidence that intermittent treatment with PTH may enhance the early fixation of orthopaedic implants. Aim of this study was the evaluation of the impact of Total Knee Replacement (TKR) on the serum level of Intact-Parathyroid Hormone (I-PTH), as continuously elevated levels of the latter may potentially play a negative role in the implant’s incorporation process.

Methods: During a period of 29 months, one hundred and nineteen postmenopausal women suffering from end-stage idiopathic knee osteoarthritis, scheduled to undergo TKR, were enrolled in this prospective study. Their mean age was 69.8 (±6.01) years. The serum levels of I-PTH, Calcium, Phosphorus & Creatinine were evaluated and the clearance of creatinine was calculated one day pre-operatively and on the seventh post-operative day. Patients with abnormal preoperative values were excluded from the study. Furthermore, patients suffering from any endocrine disorder, rheumatoid or any other secondary arthritis, osteoporosis or any other disease that could interfere with their bone homeostasis as well as patients receiving medication affecting bone metabolism, were also excluded from the study. None had suffered any fracture or underwent any orthopaedic surgical operation during the 36 months prior to their enrollment.

Results: Sixteen patients (13.4%) had abnormally elevated post-operative I-PTH values. However, statistical analysis revealed a statistically significant trend towards decrease in post-operative I-PTH values (p=0.018). The weight (p=0.763), age (p=0.776), serum creatinine level (p=0.922) and creatinine clearance of the patients (p=0.963) did not have a statistically significant impact on the observed alteration of I-PTH values after TKR.

Discussion and Conclusion: The serum levels of I-PTH seem to decrease following a TKR. This is more or less expected, as immediately after implantation, bone cells adjacent to the implant are likely to be dead due to necrosis or apoptosis. The latter is a strong stimulus for bone resorption that probably leads to increased serum calcium concentrations that may well decrease the endogenous PTH production. Another possible explanation could be the temporary immobilization of the patients undergoing TKR. However, a substantial number of women had abnormally elevated post-operative I-PTH values. Regardless of what actually caused that increase, the negative impact of continuously elevated PTH on bone formation, may interfere with the implant’s incorporation procedure, hence the evaluation of serum I-PTH before and after TKR is strongly recommended.