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bone and cartilage

Cover illustration Inset, lumbar vertebrae of a newborn mouse stained with alcian blue (cartilage) and alizarin red (bone). Background, chondrocytes in the phalange of a newborn mouse; blue coloration signals expression of 'digit genes' of the HoxD gene cluster. (Courtesy of Marie Kmita, Jozsef Zakany and Denis Duboule.)

Bone and cartilage comprise the skeleton — a finely patterned structure that provides mobility, protection of vital organs, and housing of the bone marrow. Because bones are the most inert and enduring of our mortal remains, it is surprising what dynamic and highly tuned organs they are during life, as they must simultaneously balance growth to achieve strength and resilience, and repair without overgrowth.

This balance is achieved by bone remodelling — an interplay of mineral deposition and resorption by specialized bone cells, which is constantly occurring on a microscopic scale throughout our bodies. An imbalance in remodelling is what leads to the debilitating loss of bone mass called osteoporosis, a condition that is estimated to afflict 200 million women world wide, and often leads to immobility and death. This and other diseases of bone and cartilage are responsible for a large portion of healthcare expenditures in developed countries — US$14 billion is spent annually on treating osteoporotic fractures in the United States alone.

These statistics emphasize the need for a better understanding of both the fundamentals of skeletal biology and the pathologies associated with it, which in addition to osteoporosis, include birth defects, genetic diseases, and rheumatoid and osteoarthritis. Indeed, as human life is prolonged by biomedical advances, the weak link in our health and longevity may become the strength of our bones and mobility of our joints.

This month's Insight presents a collection of articles that explore some key elements of skeletal biology, including how skeletal structures are patterned and bones and cartilage develop, the influence of genetics over human skeletal biology, the signalling pathways and transcription factors that control bone mass, and the pathogenic mechanisms of rheumatoid arthritis.

We are pleased to acknowledge the financial support of the National Institutes of Health in producing this Insight. As always, Nature carries sole responsibility for all editorial content and peer-review.

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DeWitt, N. bone and cartilage. Nature 423, 315 (2003).

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