A review of pinealectomy-induced melatonin-deficient animal models for the study of etiopathogenesis of adolescent idiopathic scoliosis.

Adolescent idiopathic scoliosis (AIS) is a common orthopedic disorder of unknown etiology and pathogenesis. Melatonin and melatonin pathway dysfunction has been widely suspected to play an important role in the pathogenesis. Many different types of animal models have been developed to induce experimental scoliosis mimicking the pathoanatomical features of idiopathic scoliosis in human.

Abnormal melatonin receptor 1B expression in osteoblasts from girls with adolescent idiopathic scoliosis.

Melatonin signaling dysfunction has been associated with the etiology of adolescent idiopathic scoliosis (AIS). Genetic analysis has also associated the occurrence of AIS with the MT2 gene. Thus, we determined whether there is abnormality in the protein expression of melatonin receptors (MT) in AIS osteoblasts.

Abnormal proliferation and differentiation of osteoblasts from girls with adolescent idiopathic scoliosis to melatonin.

Melatonin deficiency has been postulated as an etiologic factors in adolescent idiopathic scoliosis (AIS). In previous studies, melatonin was shown to regulate skeletal growth and bone formation in both humans and rats. Although it remains controversial whether there are differences in serum melatonin level between AIS and control subjects, melatonin signaling pathway dysfunction in osteoblasts has been reported in patients with AIS.

Correlation of Risser sign, radiographs of hand and wrist with the histological grade of iliac crest apophysis in girls with adolescent idiopathic scoliosis.

Study Design: A correlation analysis between histologic grade (HG) of iliac crest apophysis and skeletal age assessments.

Objective: To study the correlation between HGs of iliac crest apophysis and the skeletal age of hand and wrist, digital skeletal age (DSA), and Risser sign in the girls with adolescent idiopathic scoliosis (AIS).

Summary Of Background Data: The evaluation of the remaining growth of the patients clinically and radiologically is highly significant in predicting the curve progression and thus influencing the treatment strategy in AIS.

Glucocorticoids suppress proteoglycan production by human tenocytes.

Background: The role of glucocortiocid injection therapy in spontaneous tendon rupture is controversial. We hypothesized that glucocorticoids suppress proteoglycan production in tendon and studied the in vitro effects of dexamethasone and triamcinolone on proteoglycan production by cultured human tenocytes.

Material And Methods: We obtained primary cultures of human tenocytes from explants of healthy human patellar tendon.

Effect of dexamethasone on cultured human tenocytes and its reversibility by platelet-derived growth factor.

Background: Many cases of tendon rupture after glucocorticoid injections have been reported in the literature. Despite previous studies on the histological and biomechanical changes in tendons after glucocorticoid injections, the role of glucocorticoid in causing tendon rupture still remains controversial. The objective of this study was to determine whether glucocorticoid has deleterious effects on the cellular metabolism and collagen production of cultured human tenocytes and the reversibility of these effects by platelet-derived growth factor-BB (PDGFBB).