Bone Growth

Postnatal growth in length of long bones of the appendicular skeleton precedes growth in diameter. Growth in length involves both cartilage and bone cells. Chondroblasts continue to proliferate at the growth plate adjacent to the epiphysis to maintain this cartilage plate throughout the growth period. Chondro-blasts produce cartilage matrix materials but gradually differentiate into chondrocytes, which produce and maintain mature matrix. As more chondroblasts arise, and accompanying newly synthesized matrix accumulates, mature matrix and chondrocytes begin to abut the diaphysis. Chondrocytes eventually die as a result of their initiation of the ossification process, which prevents diffusion of nutrients to cartilage cells. Ossification of cartilage results in invasion of capillaries, osteoblasts, and, ultimately, osteocytes to further bone formation adjacent to the diaphysis, thus extending its length.[3,4] While a growth plate is present at both the proximal and the distal ends of long bones, the extent of growth is not the same at each end. The differential growth rate varies among bones of an animal, e.g., in some bones the proximal end predominates and in others the distal end does.

Long bone growth in diameter occurs as osteoblasts proliferate along the outer surface of the diaphysis beneath the periosteum surrounding the diaphysis. Deposition of bone on the outer diaphyseal surface is appositional growth. It results from activity of osteoblasts and os-teocytes laying down compact bone, thereby increasing bone density and strength. Simultaneously, mononuclear precursors of osteoclasts originate in the diaphyseal o>

Time

Fig. 1 Idealized growth curves for large and small framed animals within a species.

marrow of the medullary cavity.[3,4] Fusion of mononu-cleated precursors forms multinucleated osteoclasts, which are responsible for bone resorption. Osteoclastic resorptive activity increases the size of the medullary cavity. Thus, long bone growth involves the highly coordinated activity of osteoblasts, osteocytes, and osteoclasts. During growth, bone formation exceeds resorption.

Onset of puberty initiates closure of the cartilage growth plate as sex hormones begin to increase. Estrogen is more effective than testosterone in initiating ossification. The earlier onset of puberty in females accounts for their smaller frame size. Castration of either males or females results in further growth in length of long bones compared with gonadally intact animals. However, closure of the growth plate of castrates eventually occurs via the action of other hormones. Complete ossification of the growth plate results in cessation of long bone growth in length. Appositional growth to increase diameter continues as added weight and other stresses require stronger, more compact bone. Remodeling of bone occurs throughout the life of the animal and is accomplished by the combined activity of the three bone cell types.[3,4]

Increases in size of the skull and axial skeleton post-natally occur by appositional growth. Osteoblasts proliferate from precursor cells located adjacent to existing bone beneath the periosteum. Osteoblasts produce matrix materials, which are deposited on the bone surfaces, thereby increasing their size and density. Osteoblasts differentiate into osteocytes to produce more mature bone matrix materials consistent with the maturation of the animal. Bones of the axial skeleton exhibit a posterior anterior gradient in maturation.

lation. Muscle fiber (myofiber) number is established prenatally, but nuclei within the sarcolemma do not synthesize DNA. Nevertheless, skeletal muscle DNA accretion generally parallels myofiber hypertrophy and muscular animals have greater muscle DNA than less muscular animals. Postnatal accumulation of myofiber DNA results from the activity of satellite cells, which are located between the sarcolemma and the basement membrane of myofibers. Satellite cells proliferate, differentiate, and fuse with preexisting myofibers, thereby contributing their DNA. Each myofiber nucleus is capable of supporting a finite cell volume. Since over 80% of skeletal muscle DNA of most species accumulates postnatally, satellite cell incorporation is obligatory for normal myo-

fiber growth.[4]

Protein accumulation in all tissues occurs when protein synthesis exceeds degradation. In skeletal muscle, fractional protein accretion, synthesis, and degradation rates are high in young animals and decline in older animals.[5] Myofiber growth in length and diameter is achieved by increases in myofibrillar proteins. Myo-fibrils increase in length by addition of sarcomeres. Addition of myofilaments and longitudinal splitting of myofibrils increase myofibril diameter and number, respectively. Growth in skeletal muscle length accompanies bone growth and precedes extensive increases in muscle diameter.

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  • reino
    What accompanies growth in length of long bones?
    6 years ago

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