Abstract
Introduction THE INTRODUCTION of the quantum concept for bone remodeling and in vivo tetracycline labeling by Frost in 1964 (1–3) has had a profound impact on histological studies of metabolic bone diseases over the last two decades. The quantum concept implies that changes in bone mass result from an imbalance between the amount of bone resorbed and formed, leading to either loss or gain of bone during the continuous remodeling of adult bone (1–3). Recently, a new dimension to the theories on bone loss emphasizing the importance of trabecular perforations in the development of osteopenia has been introduced by Parfitt (4). This theory explains the profound disintegration of the trabecular network occurring in certain disease states characterized by high bone turnover and increased resorptive activity (e.g. postmenopausal osteoporotic women with spontaneous vertebral fractures) and may also explain part of the bone loss that occurs with increasing age.