Osteoporosis and Bone Regeneration

Majority of skeletal conditions generate or heal normally due to inherent capacity. However, compromised conditions such as induced by congenital or acquired diseases may sometimes lead to uncompleted development or regenerate. The quality and volume of bone is an important factor to be considered in orthopaedic and dental fields. We occasionally encounter difficult clinical cases because of insufficient bone. Bone is a tissue that is being constantly remodelled, and bone mass at any given time depends on the balance between the rate of osteoblastic bone formation and osteoclastic bone resorption. These cellular functions are controlled by various systemic and local factors. Osteoporosis is a skeletal disease characterized by low bone mass and microarchitectural deterioration of bone tissue with a consequent increase in bone fragility and susceptibility to fracture (1993). The term osteoporosis was first introduced in France and Germany during the last century, meaning “porous bone” and initially implied a histological diagnosis, but was later refined for bone which was normally mineralized but reduced in quantity. Estrogen deficiency in postmenopausal women elicits bone loss in the vertebrae and long bones resulting in bone fractures, and this condition is called postmenopausal osteoporosis (T.J. Wronski et al., 1985, 1988, 1989a). To the anatomical site features, a bone defect repair rate is mainly dependent on the bone wound size (J.P. Schmitz & J.O. Hollinger, 1986). Theoretically, an experimental osseous injury performed to study repair mechanisms should be wide enough to preclude a spontaneous healing. In order to do this, the non-regeneration threshold of bone tissue was investigated in the studied models, inducing a so-called critical-sized defect (CSD). The CSD may be defined as “the smallest size intraosseous wound in a particular bone and species of animal that will not heal spontaneously during the lifetime of the animal” (J.P. Schmitz & J.O. Hollinger, 1986; J.O. Hollinger & J.C. Kleinschmidt, 1990). The CSD may be therefore considered the prototype of discontinuity defects, as a condition of failed osteogenesis for overcoming the threshold of physiologic repair processes. Although autologous or allogous bone transplant is partially effective, a simple and effective method for bone augmentation and regeneration is clinically desired in the orthopedic and dental fields. In the 1960s, Urist proposed the existence of bone-inducing molecules, which he termed bone morphogenetic proteins (BMP) (M.R. Urist, 1965). In 1988, the cDNA of BMPs was characterized, and human recombinant BMP2 (rhBMP2) (H.D. Zegzula et al., 1997; D.L. Wheeler et al., 1998; R.D. Welch et al., 1998; J.R. Lieberman et al., 1999; J.L. Dragoo et al., 2003) and BMP7 (X. Chen et al., 2002; F.C. den Boer et al., 2003; M.M. Abu-Serriah et al., 2004) are currently available. However, large amounts of rhBMP2 or 7 are required for