Does the epiphyseal cartilage of the long bones have one or two ossification fronts?
The epiphyseal plate is the area of growth in a long bone. . what are the similarities and differences between a primary and a secondary ossification center?. Mechanical loading of the bone is important for epiphyseal plate physiology. of endochondral ossification requires a constantly moving interface between relationship and to the hormonal control of the body's growth . Learn more about Epiphyseal Plate of appearance and fusion of centres of ossification to telephone numbers, being sufficiently haphazard that recourse . Some experiments on the possible relationship between vitamin C and calcification.
Capillaries and osteoblasts from the diaphysis penetrate this zone, and the osteoblasts secrete bone tissue on the remaining calcified cartilage. Thus, the zone of calcified matrix connects the epiphyseal plate to the diaphysis. A bone grows in length when osseous tissue is added to the diaphysis. Bones continue to grow in length until early adulthood. The rate of growth is controlled by hormones, which will be discussed later.
When the chondrocytes in the epiphyseal plate cease their proliferation and bone replaces all the cartilage, longitudinal growth stops. As a bone matures, the epiphyseal plate progresses to an epiphyseal line.
This growth by adding to the free surface of bone is called appositional growth. Appositional growth can occur at the endosteum or peristeum where osteoclasts resorb old bone that lines the medullary cavity, while osteoblasts produce new bone tissue.
Bone Formation and Development | Anatomy & Physiology
The erosion of old bone along the medullary cavity and the deposition of new bone beneath the periosteum not only increase the diameter of the diaphysis but also increase the diameter of the medullary cavity. However, in adult life, bone undergoes constant remodeling, in which resorption of old or damaged bone takes place on the same surface where osteoblasts lay new bone to replace that which is resorbed.
Injury, exercise, and other activities lead to remodeling. Those influences are discussed later in the chapter, but even without injury or exercise, about 5 to 10 percent of the skeleton is remodeled annually just by destroying old bone and renewing it with fresh bone.
Diseases of the…Skeletal System Osteogenesis imperfecta OI is a genetic disease in which bones do not form properly and therefore are fragile and break easily. It is also called brittle bone disease. The disease is present from birth and affects a person throughout life. The severity of the disease can range from mild to severe. Those with the most severe forms of the disease sustain many more fractures than those with a mild form.
Frequent and multiple fractures typically lead to bone deformities and short stature. Bowing of the long bones and curvature of the spine are also common in people afflicted with OI. Curvature of the spine makes breathing difficult because the lungs are compressed. Because collagen is such an important structural protein in many parts of the body, people with OI may also experience fragile skin, weak muscles, loose joints, easy bruising, frequent nosebleeds, brittle teeth, blue sclera, and hearing loss.
what is the relationship between ossification and the epiphyseal plate? | Yahoo Answers
There is no known cure for OI. Treatment focuses on helping the person retain as much independence as possible while minimizing fractures and maximizing mobility. Toward that end, safe exercises, like swimming, in which the body is less likely to experience collisions or compressive forces, are recommended.
Braces to support legs, ankles, knees, and wrists are used as needed. Canes, walkers, or wheelchairs can also help compensate for weaknesses.
When bones do break, casts, splints, or wraps are used. In some cases, metal rods may be surgically implanted into the long bones of the arms and legs.
Research is currently being conducted on using bisphosphonates to treat OI. Smoking and being overweight are especially risky in people with OI, since smoking is known to weaken bones, and extra body weight puts additional stress on the bones. Section Review All bone formation is a replacement process. Typical of a hormone secreted by the adenohypophysis, GH secretion is regulated by hormones that are secreted by parvocellular cells in the hypothalamus. A special feature is that there is both a stimulatory hormone, growth hormone releasing hormone GHRH and an inhibitory hormone, somatostatin.
There are also several other hormones that are regulators of growth. Thyroid hormone is important for growth because it promotes growth hormone synthesis. Gonadal steroids estrogen and testosteronewhose secretion increases at puberty, initially promote growth by increasing GH secretion, and then subsequently cause growth to end by causing the closure of the epiphyseal growth plates.
Cortisol, which is released in response to stress, causes an inhibition of growth. Disorders Short stature can be caused by a defect in GH secretion growth hormone deficiencybut it may also be caused by a defect in the growth hormone receptor growth hormone resistance. Growth hormone resistance is also called Laron syndrome.
Hypersecretion of GH by a pituitary tumor causes different disorders according to when during life the hypersecretion begins. Rarely, GH hypersecretion begins before closure of the epiphyseal plates. This disorder, known as gigantism, causes excessive growth of the long bones and abnormally tall stature. GH hypersecretion that starts after adulthood is called acromegaly.
Acromegaly has an insidious onset due to the fact that GH-secreting tumors are slow growing. High levels of GH and IGF-1 cause excessive growth of soft tissues and appositional growth in certain bones, particularly the jaw and skull, leading to disfiguring facial changes. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Background Children need physical activity and generally do this through the aspect of play. Active play in the form of organized sports can appear to be a concern for parents.
Clinicians should have a general physiological background on the effects of exercise on developing epiphyseal growth plates of bone. The purpose of this review is to present an overview of the effects of physical activity on the developing epiphyseal growth plates of children.
Methods A National Library of Medicine Pubmed search was initiated using the keywords and combinations of keywords "growth plate", "epiphyseal plate", "child", "exercise", and "physical activity. The normal functioning of the epiphyseal growth plate is an important clinical aspect.
Much of the physiology of the epiphyseal growth plate in response to exercise includes the important mechanical component. Growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin are seen as key physiological factors.
While there is a need for children to participate in physical activity, clinical consideration needs to be given to how the epiphyseal growth plate functions.
Conclusions Mechanical loading of the bone is important for epiphyseal plate physiology. Exercise has a healthy function on the normal growth of this important biomechanical feature. Clinically, over-exertion in the form of increased load bearing on the epiphyseal growth plate creates an ideal injury.
There is a paucity of research on inactivity on the epiphyseal growth plate resulting in stress deprivation. Further research should take into consideration what lack of exercise and lessened mechanical load bearing has on the function of the epiphyseal growth plate. Keywords Child; Physical activity; Epiphyseal growth plates; Bone; Exercise; Mechanical loading Introduction Bone has been described as a dynamic and highly interactive complex of many cell and tissue types [ 1 ]. The epiphyseal growth plate is made of several key aspects including cartilaginous, bony, and fibrous components, which act together to achieve longitudinal bone growth [ 2 ].
The epiphyseal growth plate is a final target organ for longitudinal growth and results from the cellular process of chondrocyte proliferation and differentiation [ 3 ]. Jaramillo and Hoffer [ 4 ] described the cartilaginous structures at the ends of growing bones as constituting the "growth mechanism".
Frost [ 5 ] noted that knowledge of epiphyseal growth plate physiology has application for several areas. The first area noted being that such knowledge aids in distinguishing mechanically competent bone from incompetent bone [ 5 ]. The second area is that this knowledge enables a person to increase and maintain bone strength during growth [ 5 ]. Finally, knowledge that bone strength, taken in its entirety, and bone health are to be understood as completely different from each other with regards to physiological responses [ 5 ].
Of particular importance to clinical practice is the knowledge that two major contributions to the development of articular cartilage are growth factors and mechanical loading [ 6 ]. A discussion of the physiological basis of epiphyseal growth plates will be included. Practitioners with a familiarity of the dynamic changes that can occur with the epiphyseal plate in normal children can ultimately lead to recognition of pathologic states [ 78 ].
A Review of the Normal Physiology of the Epiphyseal Growth Plate As noted previously, skeletal growth at the epiphyseal plate is an active and dynamic process [ 8 ]. The epiphyseal growth plate, being a highly specialized layer of cartilage where chondrocytes proliferate and differentiate, brings forth longitudinal bone growth [ 9 ].
The epiphyseal growth plate can be divided into three main chondrocyte subpopulations: Longitudinal bone growth is primarily achieved through the action of chondrocytes in the proliferative and hypertrophic zones of the growth plate [ 11 ]. Longitudinal bone growth occurs in the epiphyseal growth plate through a process called endochondral bone formation and ossification [ ]. Endochondral bone formation is a process where resting zone chondrocytes are recruited to start active proliferation and then undergo differentiation, followed by mineralization [ 12 ].
Production of metaphyseal cancellous bone and growth in length are both linked to endochondral ossification with growth plate cartilage cell proliferation as the driving force [ 15 ]. Within the epiphyseal growth plate, chondrocyte proliferation, hypertrophy, and cartilage matrix secretion result in chondrogenesis [ 14 ].
Endochondral bone development leading at the epiphyseal growth plate contributes to longitudinal bone growth through a process through which undifferentiated mesenchymal cells differentiate into chondrocytes, which then undergo well-ordered and controlled phases of proliferation, hypertrophic differentiation, death, blood vessel invasion, and finally replacement of cartilage with bone [ 16 ].
The newly formed cartilage is invaded by blood vessels and bone cells that remodel the newly formed cartilage into bone tissue [ 14 ]. The regulation of linear bone growth in children and adolescents comprises a complex interaction of hormones and growth factors [ 17 ].
This process of longitudinal bone growth is governed by an intricate network of endocrine signals, including growth hormone, insulin-like growth factor I, glucocorticoid, thyroid hormone, estrogen, androgen, vitamin D, and leptin [ 14 ]. Many of these signals act locally on growth plate chondrocytes to regulate epiphyseal growth plate function [ 14 ]. The regulation of longitudinal growth at the epiphyseal growth plate occurs generally through the intimate interaction of circulating systemic hormones and locally produced peptide growth factors which has the net result of triggering changes in gene expression by growth plate chondrocytes [ 13 ].
In particular, for the majority of skeletal elements to develop and grow, the process of endochondral ossification requires a constantly moving interface between cartilage, invading blood vessels, and bone [ 1 ]. The active metabolite of vitamin D, 1,dihydroxyvitamin D 1,25 OH 2Dis classically appreciated to exert its calcemic and other actions via interaction with the vitamin D receptor thus modulating gene transcription [ 19 ]. However, with respect to parathyroid gland function and development of the cartilaginous epiphyseal growth plate, calcium and 1,25 OH 2D act cooperatively and 1,25 OH 2D will act independently of the vitamin D receptor [ 19 ].
The balance between proliferation and differentiation in bone is considered to be a crucial step. It is a crucial regulatory step controlled by various growth hormones acting in the endocrine pathways [ 12 ]. Growth hormone GH and insulin-like growth factor-I have major effects on the chondrocytes of the growth plate and act upon all bone cells [ 20 ].
Growth hormone GHmostly seen in action during the growth spurt in early adolescence, is considered to be the key hormone regulator of linear growth during childhood [ 17 ]. Research with laboratory animals has provided most of the current information regarding estrogen's influence on the growth process of long bones, on the maintenance of cancellous bone mass, and on the architectural and cellular changes in bone [ 21 ]. Estrogen action is indispensable for normal pubertal growth and growth plate fusion.
Both estrogen receptors ERER-alpha and ER-beta, are expressed in the growth plate in boys and girls throughout pubertal development [ 12 ]. The rise in estrogen levels at menarche in girls is associated with a large reduction in bone turnover markers and reflects the closure of the epiphyseal growth plates, the reduction in periosteal apposition and endosteal resorption within cortical bone [ 22 ].
Jarvinen [ 23 ] noted that estrogen tends to pack mechanically-excess mineral into the female skeleton at puberty thus creating the paradigm that the most responsive period of female bone to mechanical loading occurs prior to menarche. This knowledge has consequence for the encouragement of physical activity especially for the female population.
As previously noted, longitudinal growth of the skeleton is a result of endochondral ossification that occurs at the epiphyseal growth plate. Through the sequential process of cell proliferation, extracellular matrix synthesis, cellular hypertrophy, matrix mineralization, vascular invasion, and eventually apoptosis, cartilage continually is being replaced by bone as length increases [ 15 ].
Parfitt [ 15 ] explained that genetic determination of bone mass is mediated by two classes of gene. The first class of gene under the control of the sizostat regulates growth of muscles and bones [ 15 ]. The second class of gene under the control of the mechanostat regulates the increase in bone density in response to load bearing [ 15 ]. With skeletal maturity, there is a decreased growth rate and is mainly associated with structural changes in the physis, including a gradual decline in growth plate width due to the reduced height of the proliferative and hypertrophic zones [ 13 ].
Mechanical Influence on the Physiology of the Epiphyseal Growth Plate Comprehension of the biomechanical aspects of bone allows one to conceptualize the physiological processes associated with exercise and physical activity on the epiphyseal growth plate. The mechanical influence on bone directly applies to the normal physiological functioning of bone.
Longitudinal growth is controlled by local mechanical factors in the form of a feedback mechanism which exists to ensure that bone growth proceeds in the direction of the predominant mechanical forces [ 11 ]. The individual epiphyses undergoes a characteristic series of events; central calcification, absorption of cartilage and endochondral ossification, the further course of which is definitely determined by the degree of local distortion [ 24 ]. Production of diaphyseal cortical bone and growth in width are both linked to periosteal apposition driven by the process of osteoblast precursor proliferation [ 15 ].
During adolescence the trabeculae and cortices become thicker by endosteal apposition which increases bone density [ 15 ]. Intrinsically, biophysical forces placed upon the bone assist to develop the growing bone while extrinsic biophysical forces tend to resist and channel the expansion of bone into its functional forms such as the internal trabecular architecture and the external shape [ 25 ].
In addition to the vital function of growth factors, it is known that mechanical forces stimulate the synthesis of extracellular proteins in vitro and in vivo and can affect the tissue's overall structure [ 7 ]. According to the mechanostat theory, periosteal apposition is regulated by biomechanical requirements [ 11 ]. The stress acting on the cartilaginous epiphysis is comparable to that in the adult with relative differences attributed to variations in the mechanical relationship and to the hormonal control of the body's growth [ 24 ].
Frost [ 5 ] noted that later-discovered tissue-level mechanisms and functions including biomechanical and muscle are the true key players in bone physiology, and homeostasis ranks below the mechanical functions. The Role of Exercise and Physical Activity on the Epiphyseal Growth Plate Over the past decade, there has been a surge in the number of sports opportunities available to young athletes [ 26 ].
Beyond the positive physiological, psychological and social aspects that a sports activity brings to adolescents, there exists the potential risk of injuries and overuse of the locomotor system [ 27 ].