Nitric oxide content and apoptosis rate in steroid-induced avascular necrosis of the femoral head

Abstract

Abstract. The aim of the present study was to explore the effect on nitric oxide (NO) content and osteocyte apoptosis of steroid-induced avascular necrosis of the femoral head (SANFH) in an animal model of SANFH. A total of 40 Japanese white rabbits, 5 months of age and weighing 2.5±0.5 kg, were randomly divided into groups A (hormone + endotoxin group), B (endotoxin + normal saline group), C (normal saline + hormone group) and D (control group). Following the establishment of the model, a blood sample was taken from the heart of each animal and centrifuged; the levels of NO in the serum were detected. The bilateral femoral heads were conventionally dissected, fixed, decalcified and stained with hematoxylin and eosin. Subsequently, the empty bone lacunae were counted under an optical microscope. Changes in osteocyte morphology were observed using electron microscopy and osteocyte apoptosis was detected with a terminal deoxynucleotidyl transferase dUTP nick end labeling assay. The percentage of empty bone lacunae in group A was significantly higher compared with that in groups B, C and D (P<0.01); however, there was no significant difference in percentage among groups B, C and D. The NO content in group A was significantly higher compared with that in groups B, C and D (P<0.01); however, there was no significant difference in NO content among groups B, C and D. The osteocyte apoptosis index in group A was significantly higher compared with that in the other groups (P<0.01); there was no significant difference among groups B, C and D. NO content was positively correlated with osteocyte apoptosis index (r=0.707). Thus, the present study found that NO content and the osteocyte apoptosis index were increased in SANFH, and that they play an important role in SANFH. The content of NO was positively correlated with the osteocyte apoptosis index, indicating that NO induces apoptosis.

ARG2, MAP4K5 and TSTA3 as Diagnostic Markers of Steroid-Induced Osteonecrosis of the Femoral Head and Their Correlation With Immune Infiltration

“…This study demonstrated that ARG2 played a role in the modulation of polyamine metabolism and nitric oxide by regulating local arginine concentrations (Vockley et al, 1996). As reported by earlier studies, the content of nitric oxide is positively linked to the index of osteocyte apoptosis, indicating that nitric oxide induced osteocyte apoptosis (Bai et al, 2015). Coincidentally, according to several studies, abnormal arginase expression displayed significant correlations with multiple pathological processes, such as ischemic stroke (Lyu et al, 2020), cardiovascular (Berkowitz et al, 2003), and immune-mediated (Morris, 2016).…”

The protective effects of microRNA-26a in steroid-induced osteonecrosis of the femoral head by repressing EZH2

“…The incidence of SONFH is correlated with the management methods and the dose of the steroid. Moreover, SONFH usually could not be early diagnosed for most patients [6]. Resulted from nonspecific symptom in the early period, patients with SONFH usually miss the best time to receive nonsurgical therapy, hence early diagnosis and therapy of SONFH remain significant [7].…”

Advances in experimental models of osteonecrosis of the femoral head

“… 15–90% [ 7 , 29 ] LPS Induce immune stimulatory factors. 9% [ 7 , [30] , [31] , [32] ] HS Induce serum sickness ONFH by injection of HS. 60–90% [ 8 , 17 , 32 , 33 ] GC ​+ ​LPS Simulate the inflammatory host state, initiate intravascular coagulation and eventual ONFH.…”

“… 60–90% [ 8 , 17 , 32 , 33 ] GC ​+ ​LPS Simulate the inflammatory host state, initiate intravascular coagulation and eventual ONFH. 50–90% [ 7 , 30 , 31 , [29] , [34] , [35] , [36] , [37] ] GC ​+ ​HS Induce vasculitis, causing breakdown and obstruction of small arteries. 90% [ 38 , 39 ] ALC Simulate alcohol-related ONFH in humans.…”