Bones can be classified into three groups: short, flat, and long or tubular.Mature bones consist of a central fatty or heamatopoietic marrow that is supported and surrounded by bone tissue and periosteum. Marrow can serve as a source of bone cells; the blood vessels in the marrow form a critical part of the circulatory system in bone, and disorders or mechanical disruption of the marrow can affect the activities of bone and periosteal cells.The periosteum contributes an important part of the blood supply to the bone.Bone cells assume specialized forms distinguished by morphology, function, and characteristic location. They orginate from two cell lines: a mesenchymal stem-cell line and a heamatopoietic stem-cell line.The formation of bone differs from the soft-tissue or bone-marrow calcification that occurs as a result of injury or disease, even though both processes result in the deposition of mineral and both may occur within the soft tissues. Although there is only one mechanism of bone formation, it may occur within cartilage (enchondral), within an organic matrix membrane (intramembranous), or by deposition of new bone on existing bone (appositional).Normal mechanical function of musculoskeletal system required not only the formation of bone tissue with the necessary composition but also creation of different bone shapes from the same tissue.After initial ossification of embryonic skeleton osteoclast and osteoblast begin modeling and remodeling each bone. In general, remodeling refer to turnover of the bone that does not alter the shape of bone whereas modeling alter shape of the bone; however, the two process often occur simultaneously and distinction between them may not be readily apparent. The rate of turnover of skeleton approaches 100% per year in the first year of life, decline to about 10%per year in late childhood and then usually continues approximately this rate or more throughout life.Modeling is strictly a process that increases the amount of bone tissue in the absence of resorption (e.g. periosteal surface apposition). Remodeling, on the other hand, changes bone morphology by the coordinated processes of bone formation and resorption (e.g.drilling and refilling of an osteon cortical drift). Remodeling is fundamental to bone biology. It is a two-stage process carried out by teams of cells known as basic multicellular units (BMUs). Resorption of a packet of bone by osteoclasts is followed by refilling of the resorption cavity by osteoblasts. This sequence typically requires 3-4 months to complete at each locus, and the resorption and refilling cavities, while individually small, may collectively add substantial temporary porosity or “remodeling space” to the bone.In modeling, bone resorption or formation at a particular site occurs independently of one another; in remodeling, resorption and formation occur in a coupled sequence. Modeling occurs primarily in children, and usually on periosteal and on endosteal surfaces. Remodeling occurs throughout life, and primarily on the haversian and trabecular surfaces of cortical and cancellous bone, respectively.There is observation that remodeling increases both when mechanical loading excessively low, that is, in a disuse state, and when it is excessively high, producing substantial fatigue damage. The new theory resolves this disparity by assuming that the lining cells are inclined to activate remodeling unless restrained by an inhibitory signal, and that mechanically provoked osteocytic signal serves this inhibitory function. Consequently, remodeling is elevated when signal generation declines due to reduced loading, or when signal generation or transmission is interrupted by damage due to excessive loading. Otherwise, remodeling is kept at a relatively low level by inhibitory signals produced through physiologic loading. A theory for the control of bone remodeling based on five fundamental hypotheses. The first is that the bone lining cells are responsible for activating bone remodeling. The second is that the osteocytic syncytium produces and transmits a signal proportional to some correlate of mechanical loading. The third is concerned with conversion of osteoblasts to osteocytes through that osteocytes send an inhibitory signal to osteoblasts that reduces their rate of bone production. The fourth is that Marotti’s inhibitory osteocytic signal is produced in response to mechanical loading, and this signal also serves to inhibit bone-lining cells from activating remodeling. The last one is in direct contrast to the widespread assumption that mechanical loading produces an osteocytic signal that activates remodeling unless inhibited by Marotti’s inhibitory signals. Abnormal bone remodeling can be produced by alteration of normal balance between formation and resorption. Abnormal bone remodeling can produce a variety of skeletal disorders.Bone remodeling is controlled by many factors either local or systemic. The most important of them are calciotropic hormones.The recent explosion of knowledge concerning systemic and local regulation of bone remodeling should lead to new approaches to the diagnosis-and treatment of skeletal disorders. New specific markers of bone remodeling have been developed that allow the evaluation of bone formation (plasma level of osteocalcin and bone alkaline phosphatase) or bone resorption (collagen cross-link levels in urine). These markers can be used to evaluate bone disease. Their best application is currently in renal osteodystrophy, where there is a broad spectrum of bone abnormalities. Bone marker measurements are non-invasive and can be repeated often. Major changes occur in short times. Markers are derived from both cortical and trabecular bone and reflect the metabolic activity of entire skeleton. Bone markers have been useful in clinical practice and have been helpful in understanding the pathogenesis of osteoporosis and the mechanism of action therapies. In clinical trials, markers aid in selecting optimal dose and in understanding the time course of onset and resolution of treatment effect. In particular, the newer methods in molecular and cellular biology should enable us to define the abnormalities in cells of the osteoblastic and osteoclastic lineages that lead to bone disease and to develop new approaches based on a fuller understanding of the pathogenetic mechanisms in these disorders.