Abstract
BackgroundAlthough, glucocorticoid (GC) and calcitonin-induced changes in bone repair have been studied previously, the exact effects of these on fracture healing remain controversial. Hence, the purpose of this experimental study is to determine biochemical and histological effects of locally administrated GC and systemically administrated calcitonin on the kinetics of healing response after bone marrow ablation in rats.MethodsAfter having undergone marrow ablation, a steroid-treated group of rats (n = 24) received a single dose of intramedullary methylprednisolone (2 mg/kg), a calcitonin-treated group (n = 24) received intermittently administrated subcutaneous salmon calcitonin (16 IU/kg), and a control group (n = 24) received intramedullary saline (25 μl).ResultsBlood samples taken on days 1, 3, 7, 9, and 15 after ablation showed an increase in serum calcium, alkaline phosphatase (ALP), and phosphate levels in the Calcitonin and Control groups. Levels of calcium and ALP peaked on day 7 after ablation. However, an increase in phosphate levels indicated a biphasic reaction that peaked on the third and ninth day after ablation. Hypercalcemia was not observed in Steroid group because of the inhibition of osteoclastic bone resorption. In that group, the serum levels of ALP and phosphate were lower than baseline levels. The levels of urinary calcium excretion peaked 3 to 7 days after marrow ablation in the control group and 7 to 9 days after that procedure in the steroid group. Histologic evaluation showed that the rats in the control group demonstrated the expected healing period according to the histological grades and that a delay in healing occurred in the calcitonin group after day 9 because of the inhibition of osteoclastic bone resorption. All rats in the steroid group exhibited a decrease and delayed healing response.ConclusionTotal serum calcium, phosphate, and ALP levels increased after bilateral tibial bone marrow ablation and urine calcium and hydroxyproline excretion also increased as a factor of bone resorption. Subcutaneously administrated salmon calcitonin did not affect biochemical changes after marrow ablation. Single-dose intramedullary methylprednisolone inhibited extra-tibial bone resorption induced by cytokines after bone marrow ablation.
Highlights
Glucocorticoid (GC) and calcitonin-induced changes in bone repair have been studied previously, the exact effects of these on fracture healing remain controversial
Mechanical bone marrow ablation (BMX) is a convenient model of intramembranous bone regeneration, in which the intramedullary bone formation occurring on postoperative days 1 to 8 is followed by the resorption of that bone and the re-establishment of red marrow tissue on postoperative days 9 to 15 (Gazit et al 1989; Gazit et al 1990; Liang et al 1992; Magnuson et al 1997; Schwartz et al 1989; Suva et al 1993)
The change in bone formation may be a direct effect of steroid treatment, but the increased osteolysis probably results from secondary hyperparathyroidism that is caused in turn by decreased intestinal calcium absorption and increased urinary calcium excretion (Hardy et al 1993; Suzuki et al 1983; Yan et al 2012; Wang et al 2002)
Summary
Glucocorticoid (GC) and calcitonin-induced changes in bone repair have been studied previously, the exact effects of these on fracture healing remain controversial. Glucocorticoid (GC) and calcitonin-induced changes in bone metabolism have been studies previously in the literature, the exact effects of these on fracture healing and resorption remain controversial due to different methodologies, heterogenous study groups, different outcome measures and non-comparative conclusions. It is very well-known in the literature that longterm treatment with GCs leads to osteoporosis caused by the inhibition of bone formation and the stimulation of bone resorption (Hardy et al 1993; He et al 2016; Hellewell et al 1974; Kang et al 2016; Shi et al 2015; Wang et al 2002).
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