Cell mechanics and cellular engineering may be defined as the application of principles and methods of engineering and life sciences toward fundamental understanding of structure-function relationships in normal and pathological cells and the development of biological substitutes to restore cellular functions. This definition is derived from one developed for tissue engineering at a 1988 NSF workshop. The reader of this volume will see the definition being applied and stretched to study cell and tissue structure-function relationships. The best way to define a field is really to let the investigators describe their areas of study. Perhaps cell mechanics could be compartmentalized by remembering how some of the earliest thinkers wrote about the effects of mechanics on growth. As early as 1638, Galileo hypothesized that gravity and of living mechanical forces place limits on the growth and architecture organisms. It seems only fitting that Robert Hooke, who gave us Hooke's law of elasticity, also gave us the word "cell" in his 1665 text, Micrographid, to designate these elementary entities of life. Julius Wolffs 1899 treatise on the function and form of the trabecular architecture provided an incisive example of the relationship between the structure of the body and the mechanical load it bears. In 1917, D' Arcy Thompson's On Growth and Form revolutionized the analysis of biological processes by introducing cogent physical explanations of the relationships between the structure and function of cells and organisms.

Historical folklore indicates that Asldepios (circa 900 BC), the fIrst western doctor of ancient Greece, treated many patients with rheumatic diseases of 1 joints ,2. Later, Hippocrates (circa 400 BC), who claimed to have learned from Asklepios, used the term arthritis in reference to joint diseases: "When the disease of arthritis strikes, acute inflammation and pain attacks the joints of the body ... ". Indeed, arthritic joint disease dates much farther back into antiquity than Asklepios. Many modern anthropologists have noted degenerative joint disease in the fossils of Neanderthal man (archanthropus europeus petraloniensis) and even in those of dinosaurs. More recent scientific studies on joints date back to the work of the great English anatomist Hunter who wrote "The Structure and Diseases of Articular Cartilage" in the Philosophical Transactions of London in 1743. The notion that osteoarthritis results from the wearing away of cartilage was copiously documented by the histological observations of the German physician Ecker in 1843. This idea was further supported by Pommer (1927) who felt that mechanical stresses played important roles in the initiation and propagation of cartilage lesions leading to osteoarthritis. This same conclusion was reached by the assembled distinguished experts at a National Institutes of Health Workshop 3 held in 1986 .

Historical folklore indicates that Asklepios (circa 900 BC), the fir~t western doctor of ancient Greece, treated many patients with rheumatic diseases of 1 joints ,2. Later, Hippocrates (circa 400 BC), who claimed to have learned from Asklepios, used the term arthritis in reference to joint diseases: "When the disease of arthritis strikes, acute inflammation and pain attacks the joints of the body ... ". Indeed, arthritic joint disease dates much farther back into antiquity than Asklepios. Many modern anthropologists have noted degenerative joint disease in the fossils of Neanderthal man (archanthropus europeus petraloniensis) and even in those of dinosaurs. More recent scientific studies on joints date back to the work of the great English anatomist Hunter who wrote "The Structure and Diseases of Articular Cartilage" in the Philosophical Transactions of London in 1743. The notion that osteoarthritis results from the wearing away of cartilage was copiously documented by the histological observations of the German physician Ecker in 1843. This idea was further supported by Pommer (1927) who felt that mechanical stresses played important roles in the initiation and propagation of cartilage lesions leading to osteoarthritis. This same conclusion was reached by the assembled distinguished experts at a National Institutes of Health Workshop 3 held in 1986 .