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    Extracorporeal Shockwave Therapy Modulates the Expressions of Proinflammatory Cytokines IL33 and IL17A, and Their Receptors ST2 and IL17RA, within the Articular Cartilage in Early Avascular Necrosis of the Femoral Head in a Rat Model
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    Abstract:
    Avascular necrosis (AVN) of the femoral head (AVNFH) is a disease caused by injury to the blood supply of the femoral head, resulting in a collapse with osteonecrosis and damage to the articular cartilage. Extracorporeal shockwave therapy (ESWT) has been demonstrated to improve AVNFH owing to its anti-inflammation activity, angiogenesis effect, and tissue regeneration in clinical treatment. However, there are still so many pieces of the jigsaw that need to be fit into place in order to ascertain the mechanism of ESWT for the treatment of AVNFH. The study demonstrated that ESWT significantly protected the trabecular bone volume fraction BV/TV (P < 0.01) and the trabecular thickness (P < 0.001), while in contrast, the trabecular number and trabecular separation were not significantly different after treatment as compared with AVNFH. ESWT protected the articular cartilage in animal model of AVNFH. The levels of IL1-β and IL33 were significantly induced in the AVNFH group (P < 0.001) as compared with Sham and ESWT groups and reduced in ESWT group (P < 0.001) as compared with AVNFH group. In addition, the expression of the receptor of IL33, ST2, was reduced in AVNFH and induced after ESWT (P < 0.001). The expression of IL17A was induced in the AVNFH group (P < 0.001) and reduced in the ESWT group (P < 0.001). Further, the expression of the receptor of IL17A, IL17RA, was reduced in the AVNFH group (P < 0.001) and improved to a normal level in the ESWT group as compared with Sham group (P < 0.001). Taken together, the results of the study indicated that ESWT modulated the expression of IL1-β, pro-inflammatory cytokines IL33 and IL17A, and their receptors ST2 and IL17RA, to protect against loss of the extracellular matrix in the articular cartilage of early AVNFH.
    Keywords:
    Extracorporeal shockwave therapy
    Proinflammatory cytokine
    Avascular Necrosis
    Sham surgery
    Receptor expression
    ObjectiveTo assess the effectiveness and safety of low-intensity extracorporeal shockwave therapy (Li-ESWT) on patients with erectile dysfunction (ED).
    Extracorporeal shockwave therapy
    Intensity
    Extracorporeal
    Citations (0)
    Avascular necrosis (AVN) of the femoral head (AVNFH) is a disease caused by injury to the blood supply of the femoral head, resulting in a collapse with osteonecrosis and damage to the articular cartilage. Extracorporeal shockwave therapy (ESWT) has been demonstrated to improve AVNFH owing to its anti-inflammation activity, angiogenesis effect, and tissue regeneration in clinical treatment. However, there are still so many pieces of the jigsaw that need to be fit into place in order to ascertain the mechanism of ESWT for the treatment of AVNFH. The study demonstrated that ESWT significantly protected the trabecular bone volume fraction BV/TV (P < 0.01) and the trabecular thickness (P < 0.001), while in contrast, the trabecular number and trabecular separation were not significantly different after treatment as compared with AVNFH. ESWT protected the articular cartilage in animal model of AVNFH. The levels of IL1-β and IL33 were significantly induced in the AVNFH group (P < 0.001) as compared with Sham and ESWT groups and reduced in ESWT group (P < 0.001) as compared with AVNFH group. In addition, the expression of the receptor of IL33, ST2, was reduced in AVNFH and induced after ESWT (P < 0.001). The expression of IL17A was induced in the AVNFH group (P < 0.001) and reduced in the ESWT group (P < 0.001). Further, the expression of the receptor of IL17A, IL17RA, was reduced in the AVNFH group (P < 0.001) and improved to a normal level in the ESWT group as compared with Sham group (P < 0.001). Taken together, the results of the study indicated that ESWT modulated the expression of IL1-β, pro-inflammatory cytokines IL33 and IL17A, and their receptors ST2 and IL17RA, to protect against loss of the extracellular matrix in the articular cartilage of early AVNFH.
    Extracorporeal shockwave therapy
    Proinflammatory cytokine
    Avascular Necrosis
    Sham surgery
    Receptor expression
    Citations (8)
    Avascular necrosis of bone or Osteonecrosis incidence has been increasing in a larger number of surviving ALL patients, especially in adolescents and young adults [1]. Osteonecrosis and decreased bone mineral density(BMD) are well-known side effects of corticosteroids and avascular necrosis has been reported as one of the leading causes of treatment related morbidity in ALL survivors [2]. Symptomatic avascular necrosis has been reported to occur in up to 20% of children and adolescents with ALL [3]. We are reporting two cases of ALL patients who have been treated with steroid and chemotherapy and developed avascular necrosis of bilateral femoral heads.
    Avascular Necrosis
    Citations (1)
    A study of the X-rays of 450 children treated for congenital dislocation of the hip revealed 56 hips with total or partial avascular necrosis of the femoral head. These hips were classified into four groups. Group 1 consisted of 13 hips in which the femoral head was normal before treatment and avascular necrosis appeared during or after orthopedic or surgical procedures. These are the iatrogenic cases. Group 2 consisted of 22 hips in which avascular necrosis was evident before any treatment. The necrosis was considered a dystrophy arising from malposition. Group 3 included 12 hips in which the avascular necrosis might have been either iatrogenic or a dystrophy due to malposition. This could not be determined because these hips were treated early, before avascular necrosis was seen on X-ray. Group 4 consisted of nine hips in which unilateral dislocation was associated with avascular necrosis of the unaffected normal side prior to any treatment of the affected hip.
    Avascular Necrosis
    Citations (5)