Pathogenesis of slipped capital femoral epiphysis: current concepts.

Since Ambrose Paré in 1572 initially described what is believed to be the first case of slipped capital femoral epiphysis (SCFE), a virtual plethora of unproven theories has evolved in the ensuing years. The most currently popular theories embrace a framework of biomechanical events versus biochemical events having impact at the time of puberty. The zone of slipping always occurs primarily through the zone of hypertrophy in a corrugated undulating fashion. All investigative studies show that the growth plate at the time of puberty is weakened in SCFE. The final common pathway appears to be a mechanical failure of the growth plate, due to a weakened state, to resist displacement. The commonly encountered large body mass coupled with an increasingly oblique physis lying in a relative degree of retroversion creates a mechanical environment that, coupled with delicate alterations in the hormonal balance of thyroid hormone, growth hormone, testosterone, and estrogen, render the plate intrinsically suspectible to displacement by rather innocuous forces occurring in a shear plane. Ultrastructure studies of SCFE demonstrate a significant alteration in anatomy and physiology in all active metabolic areas of the growth plate. It is the author's concept that SCFE is a generalized metabolic disorder of puberty resulting from a series of pubertal mishaps with a multifactorial basis ordinarily caused by a relative imbalance of hormones, coupled with biomechanical events.