Treatment of primary osteoporosis has advanced dramatically during the past decade, with more therapeutic options being available now than at any other time. Anti-resorptive (anti-catabolic) drugs have been prominent in the treatment of osteoporosis for decades. However, over time, several clinical observations made during use of these agents have challenged the prevailing dogma about mechanisms of drug action, changes in bone density and fracture reduction during treatment. It has become clear that changes in bone density are only a small part of the explanation for the dramatic reduction of fractures with treatment. From this paradox developed the notion of 'bone quality'- an operational term describing a number of characteristics that enable bone to resist fracturing. This article reviews this concept from a clinical perspective. It discusses the historical paradoxes found in clinical practice that have led to this notion, identifies the major areas of bone physiology circumscribed by the concept and focuses on present therapies and their effects on bone quality.