The Development and Growth of Bones - Essay Example

Skeletal System Essay DESCRIBE THE DEVELOPMENT AND GROWTH OF BONES Ossification or osteogenesis begins towards the end of 8th week of gestation. All bones begin as mesenchymal condensations during the embryonic period. The fibrous condensations ossify into the membrane or dermal bones and the cellular condensations ossify in to hyaline cartilages (Gardner, 856-862). Thus, the skeletal pattern is formed in cartilage and connective tissue membranes. From here, bone development continues throughout adulthood. The 3 cell types involved in the development, growth and remodeling of bones are osteoblasts, osteocytes and osteoclasts. While osteoblasts are bone-forming cells, osteocytes are mature bone cells and osteoclasts break down and reabsorb bone (”Bone Growth and Development”). Ossification is basically of 2 types, intramembranous and endochondral. In both these, the formation of bone tissue is similar. First, there is increase in the number of cells and collagen fibers. Then, the cells differentiate into osteoblasts. These cells form an organic matrix called the osteoid in which the bone salts are deposited. Some of these osteoblasts remain in the matrix and transform into osteocytes (Gardner, 856-862). The replacement of sheet-like connective tissue membranes with bony tissue is known as intramembranous ossification and bones formed by this method are known as intramembranous bones. Some of the flat bones of the skull and irregular bones fall into this category. These bones are initially formed as connective tissues membranes, later on the osteoblasts migrate to the membranes and deposit bony matrix around themselves and change into osteocytes. Replacement of hyaline cartilage with bony tissue is known as endochondral ossification. Most of the bones in our body are formed in this manner and hence these bones are known as endochondral bones. The bones are first formed as hyaline cartilage models as early as in the 3rd month of gestation. This is surrounded by a membrane called the perichondrium. Later, this becomes infiltrated with blood vessels and osteoblasts and then is called the periosteum (”Bone Growth and Development”). Bone grows only by laying down of new bone on free surfaces. This is known as apposition. Another important process in the growth of bones is resorption of bone which is done by the osteoclasts. Primary center of ossification is the region in the bone in which the process of ossification starts first and this is indicated by an increase in the cells and fibers. Ossification continues from this center toward the ends of the bones. The time at which the primary center appears depends on the bone. The parietal and frontal bones, maxilla, and mandible appear during the embryonic period. In the long bones, the primary center of ossification is in the diaphysis. The diaphysis is the main or the shaft of a long bone. During ossification of the diaphysis, osteoblasts form a collar of compact bone around the diaphysis and the cartilage in the center of the diaphysis begins to disintegrate (”Bone Growth and Development”). Osteoblasts penetrate the disintegrating cartilage and replace it with spongy bone. Ossification continues from this center toward the ends of the bones. Once the spongy bone is formed, osteoclasts break down the newly formed bone to open up the medullary cavity (”Bone Growth and Development”). The rounded end of a long bone is known as epiphysis. The cartilage in the epiphyses continues to grow so the developing bone increases in length. Secondary ossification centers form in the epiphyses after birth. During ossification in the epiphysis, the spongy bone is retained instead of being broken down to form a medullary cavity (”Bone Growth and Development”). The metaphysis is the portion of a long bone between the epiphyses and the diaphysis. When secondary ossification is complete, the hyaline cartilage is totally replaced by bone except in two areas. A region of hyaline cartilage remains over the surface of the epiphysis as the articular cartilage and another area of cartilage remains between the epiphysis and diaphysis. This is the epiphyseal plate or growth region (”Bone Growth and Development”). Growth in these regions increases the length of the bone. Bone growth is under the influence of growth hormone from the anterior pituitary gland and sex hormones from the ovaries and testes (”Bone Growth and Development”). DESCRIBE THE FACTORS WHICH AFFECT THE MINERAL CONTENT OF BONE DURING THE HUMAN LIFE SPAN, AND THE CONSEQUENCES OF LOW BONE MINERAL CONTENT. The adult skeleton continually undergoes a process of bone remodeling by which old bone is removed and replaced by new bone (Cosman, “Medscape today”). In the young adult, the amount of bone replaced is equivalent to the amount removed. With aging in both sexes, the balance between resorption and formation is such that more bone is removed than replaced (Cosman, “Medscape today”). In women during menopause, there is an increase in the rate of bone remodeling and there is tremendous imbalance between formation and resorption due to decrease in estrogens and though this slows after menopause, it continues throughout the latter decades of life and rates of loss increase again in very old age (Cosman, “Medscape today”). In men, age-associated decline in their ability to aromatize androgens to estrogens is the cause. Other causes of age related bone loss include reduced renal calcium conservation efficiency, decreased vitamin D supply and decreased renal activation of vitamin D (Cosman, “Medscape today”). Bone density reaches a peak during late adolescence and is determined primarily by genetic factors (Cosman, “Medscape today”). Environmental and lifestyle factors also do play a role in bone mass. Adequate dietary intake during the growth period may be critical in reaching bone growth potential (Eustice, “Osteoporosis”). Peak bone mass tends to be higher in men than in women. This difference is due to higher androgen levels resulting in greater periosteal apposition in adolescent boys and estrogen inhibiting this apposition in adolescent girls (Cosman, “Medscape today”). However, before puberty, boys and girls acquire bone mass at similar rates. African American females tend to achieve higher peak bone mass than Caucasian females (Cosman, “Medscape today”). Estrogen has an effect on peak bone mass. Hence, women who had their first menstrual cycle at an early age and those who use oral contraceptives which contain estrogen have higher bone mineral density (Cosman, “Medscape today”). Also, reduced bone mass is seen in women with amenorrhea from a variety of causes, including excessive exercise, anorexia nervosa and hyperprolactinemia (Cosman, “Medscape today”). Calcium deficiency in the diet leads to decreased density in bones. Studies have shown that replacing milk intake by soft drinks appears to be detrimental to bone gain (Whiting, 696-700). Girls and boys and young adults who exercise regularly generally achieve greater peak bone mass than those who do not. The best exercise for the bones is weight-bearing exercise. Smoking, alcohol and sedentary life styles cause low bone density (Eustice, “Osteoporosis”). Many chronic diseases, and medications like antiepileptics, excessive thyroid hormone, chemotherapy, and gonadotropin-releasing hormone antagonists cause a decrease in bone mass (Cosman, “Medscape today”). Decreased bone mass leads to reduced bone strength, a condition known as osteoporosis where the person is susceptible to fractures secondary to minor or no trauma. DESCRIBE THE COMPOSITION AND STRUCTURE OF COMPACT BONE. There are basically 2 types of bones, the cortical or compact bones and the cancellous or spongy bone. Cortical (also known as compact) bone is found along the shafts of the long bones (femur, tibia, radius, ulna) and is the principal component of the flat bones (skull and ribs). Cancellous bone is found principally in the vertebrae of the spinal column and at the epiphyses of the long bones (Moore, “Bone”). Whatever is the type, bone is made up of three primal tissue layers: periosteum, compact bone, and spongy bone. The periosteum is a double layered tissue which covers the hard bone. It can not be seen by the naked eye. It serves as a place where tendons and ligaments can insert and anchor into the bone. The hard part of the bone is the compact bone. Microscopically it is very hollow and contains canals called canaliculi which are filled with blood vessels. These traverse through the bone and are in connection with major canals called the Haversian canals. The hardness of the bone is made up of osteocytes, mature bone cells, which surround the canaliculi and Haversian canals. The compact bone is also rich with nerves. Towards the center of the bone, the bone gets hollower and is known as spongy bone. In this there is red marrow which is rich in red blood cells; and yellow marrow in which fat is stored (“The Skeletal System”). Chemically, bone is a composed of organic and inorganic phases. Water accounts for approximately 20% of the wet weight of bone whilst about 75% of the dry weight is organic material (Moore, “Bone”). The organic material that is present is the collagen and non-collagenous protein. The inorganic substance which is present in the matrix of the bone is hydroxyapatite, a crystalline substance comprising of calcium, phosphate and hydroxyl ions. Small amounts magnesium, fluoride, carbonate, citrate and potassium as well as other ions are also found in the mineralized bone (Moore, “Bone”). References “Bone Growth and Development.” 14 Oct. 2007. Available from Cosman, F. “The prevention and treatment of osteoporosis: A review.” Medscape Today 2005. 14 Oct. 2007. Available from Eustice, C. “Osteoporosis: Factors Affecting Peak Bone Mass.” 14 Oct. 2007. Available from Gardner, ED. “The Development and Growth of Bones and Joints.” J Bone Joint Surg Am. 1963, 45: 856-862. 14 Oct. 2007. Available from Moore, RJ. “Bone.” 14 Oct. 2007. Available from “The Skeletal System.” 14 Oct. 2007. Available from Whiting, SJ, Vatanparast, H, Jones, AB, et al. “Factors that affect bone mineral accrual in the adolescent spurt.” J. Nutr. 2004. 134:696S-700S. Read More