Presentation on theme: "Histology of bone tissue premed II. Bone - specialised connective tissue."— Presentation transcript:
Histology of bone tissue premed II
Bone - specialised connective tissue
Specialised connective tissue composed of intercellular calicified material (bone matrix). Reservoir of calcium, phosphate and other ions that can be released or stored in a controlled fashion to maintain constant concentrations of these important ions in the body fluids.
Bone – General Feature -shaft- diaphysis -end epiphysis -junction of epiphysis and diaphysis – metaphysis -central medullary cavity -outercovering – periosteum -inner covering - endosteum
Forms of bone tissue 1.Embryonic bone / primary bone/woven bone/non-lamellar bone 2. Adult bone/ secondary bone /lamellar bone
This is the first bone to appear in embryonic development and in fracture repair or other repair processes.
Woven bone: -formed during development and repair -randomly arranged collagen fibre bundles -more cellular; randomly arranged -show intense staining with basic stain – abundant ground substance -found in adult where remodeling occurs -regular feature of alveolar socket
Adult bone: lamellar bone -regular arrangement of collagen fibres as sheets (lamellae) -cells oriented with their long axis parallel to the long axis of the fibre bundles -harder than the woven bone -all mature bone are lamellar in type -Osteoblasts are synthesizing collagen, Which forms a strand of matrix to trap cells, As this occurs, the osteoblasts gradually -Diffrentiate to become osteocytes.
Bone tissue – structure -is a specialised connective tissue for support, movement, to provide area for muscle attachment, form protective case for vital organs, give form and shape to the body, form store house for minerals - Components: -organic: extracellular matrix - ground substance : proteoglycans (chondroitin sulphate) -fibres – collagen type I -cells: -osteocytes (bone cells) - osteoblasts (bone + germ) bone forming cells -osteoclasts (bone + broken) for bone resorption **inorganic components of bone also depends on the presence of viable osteoblasts
Formed bone osteoid osteoblasts marrow Bone formation by osteoblasts
Osteoclasts: -large giant cell belong to mononuclear phagocyte system -developed from bone marrow -motile cells -multinucleated - lie in Howship’s lacuna on the surface of the bone
presents ruffled border (small cytoplasmic infoldings) on the surface adjoining the bone -cytoplasm adjoining the ruffled border is clear and devoid of organelle but rich in actin filaments (zone of attachment of the osteoclasts to the bone surface) --secrete collagenase that dissolves collagen fibres and liberate calcium from bone - acidic microenvironment that is created along the ruffled border by the accumulation of protons; lysosomal enzymes liberated from lysosome facilitates the dissolution of calcium which is taken by the cell and released into the blood stream.
Hormonal control of osteoclastic activity: -osteoclasts have receptors for calcitonin (thyroid hormone) -osteobalsts have receptors for paratharmone (parathyroid hormone) - when activated by paratharmone,osteoblasts releases cytokine – osteoclasts stimulating factor -osteoclasts are activated by cytokine and act on bone to liberate minerals -*bone has 99% of the body calcium in it; liberation and storage of which depends on the blood content of it -both osteoblasts and osteoclast play a balanced role in mineralisation and demineralisation of the bone to maintain blood calcium level – calcium homeostasis -What is the role of calcitonin on osteoclasts?
-Causes for abnormal bone formation: -1. Osteomalacia: soft bone due to defective mineralisation leading to reduction in calcium / organic matrix ratio - bone becomes transparent to X-rays -I). newly formed bone is not calcified -II). decalcification of already formed bone - III). may lead to abnormal deposition of calcium in kidney and blood vessel - a. dietary deficiency of calcium - b. hyperparathyroidism - c. Vitamin D deficiency – leading failure of calcium uptake by the intestine
Osteoporosis: -decrease in bone mass due to insufficient bone formation or increased bone resorption by osteoclasts - calcium/ organic matrix ratio is normal but the overall mass of the bone is reduced. Osteopetrosis: marble bone - normal bone formation with absence of osteoclastic activity resulting in overgrowth and thickening of bone; may be fatal as blood formation by the bone marrow may be impaired.
Hormonal regulation of bone formation: 1.Paratharmone (for calcium mobilisation from bone) and calcitonin (inhibitory action on osteocalsts) for balanced mineralisation of bone and to maintain calcium homeostasis 2.Growth hormone (somatotropin) from pituitary stimulates the growth of the epiphyseal cartilage-(IGF-1) - over secretion causes gigantism in children - lack of secretion causes dwarfism in children - over secretion in adult causes acromegaly – abnormal thickening 3. Thyroid hormone – deficiency of which leads to cretinism (dwarfism) 4. Sex hormone : in excess causes retardation of bone growth as epiphyseal cartilage is ossified quickly; if deficient will cause tall stature.
Children who are hypothyroid from birth are called “cretins”.showed by thyroid hormone deficiency in children,associated with dwarfism due to arrested physical development and also mental development. SEX HORMONES: -Influences the time of appearance and development of ossification centers and accelerate the closure of epiphysis. -Precocious sexual maturity : Caused by sex hormone producing tumors, retards body growth since the epiphyseal cartilage is quickly replaced by bone(closure of epiphysis). In hormonal deficiencies caused by castration or by abnormal development of gonads,the epiphyseal cartilage remains functional for a longer period of time, resulting in a tall stature.
Pathology: 1.Rickets – (in children) calcium deficiency- matrix does not calcify and deformation of already formed bone 2.Osteomalacia- soft bone (in adult)- decrease in amount of calcium per unit of bone matrix 3. Osteoporosis: reduction of both matrix and mineral level due to excessive resorption of bone ; develops as a consquence of immobilisation and postmenopausal women 4. Osteopetrosis: lack of osteoclastic activity resulting in defective resorption and so dense, heavy bone (marble bone) – genetic disorder which involves absence of ruffled borders.
Parathyroid hormone: Activates and increases the no of (osteoclasts),promoting resortion of the bone matrix with the consequent liberation of calcium. Calcitonin hormone: -Sythesized mainly by the parafollicular cells of the thyroid gland,inhibits matrix resorption. -Calcitonin has an inhibitory effect on osteoclast activity. Anaemia and frequent infections can result from depress blood cell formation. Since the concentration of calcium in tissues and blood must be kept constant,nutritional deficiencies of calcium results in decalcification of bones;decalcified bones are more likely to fracture and are more transparent to x-rays. rickets:due to defc. Of calcium in children. A disease in which bone matrix does not calcify normally and the epiphyseal plate becomes distorted.
Pathology: 1.Rickets – (in children) calcium deficiency- matrix does not calcify and deformation of already formed bone 2.Osteomalacia- soft bone (in adult)- decrease in amount of calcium per unit of bone matrix 3. Osteoporosis: reduction of both matrix and mineral level due to excessive resorption of bone ; develops as a consquence of immobilisation and postmenopausal women 4. Osteopetrosis: lack of osteoclastic activity resulting in defective resorption and so dense, heavy bone (marble bone) – genetic disorder