OSSA

DR. yan effendi hasjim, dahk2014OSSAFUNCTION OF BONE FISICAL AND MECHANICAL FUNCTIONS GREAT STRENGTH & HARDNESS STRUKTURE AND ORGANISATION (1)

METABOLIC AND HOMEOSTATIC FUNCTIONSQUITE RESPONSIVE TO MERTABOLIC, (MOBILIZABLE Ca, HOMEOSTATIC IMPORTANT IONS) CONTINOUS RENEWED AND RECONSTRUTIZED THROUHOUT THE LIFE TIMECONTINOUS INTERNAL REORGANIZATION AND RESPONSIVENESS TO EXTERNAL MECHANICAL FORCE DYNAMIC LIVING MATERIAL RESORPTION, REMODELING, RECOVERY (2)

HEMOPHOETIC FUNCTIONS BONE MARROW (3)

BONE = HARDNESS, STRENGLY AND DYNAMIC TISSUE ORGANIZATIONHISTOFISIOLOGY OF BONEMICROSTRUCTURE OSTOGENESIS, GROWTH AND DEVELOPMENTRESORPTION OF BONEREMODELING OF BONEREPAIR OF BONE DISEASES OF BONE1. ORGANIZATIONA LONG BONE EPHYPISE, DIAPHYSE, METHAPHYSE PLAT (GROWTH)PARS COMPACTA, PARS SPONGIOSA /CALCANEOUSPERIOSTEUM, ENDOSTEUMCAVUM MEDULLARECARTILAGE ARTICULATIONOSTEOGENESIS ENCHONDRALES

A FLAT BONE OF THE SKULL (SKULL CAP)INNER & OUTER TABLES, (COMPACT BONES),MIDLE THICK LAYER , DIPLO (SPONGY BONE), LABYRINTH MADULLAREOSTEOGENESIS INTRAMEMBRNOUS2. HISTOFISIOLOGY OF BONEHOMEOSTATIC, MAINTENANCE BLOOD LEVEL OF Ca (RESORPTION & DEPOSITION MATRIX)CONTINOUS RENEWED AND RECONSTRUTIZED THROUHOUT THE LIFE TIME (INTERNAL REMODELING)CONTINOUS INTERNAL REORGANIZATION AND RESPONSIVENESS TO EXTERNAL MECHANICAL FORCE (ANATOMICAL REMODELING) HEMOPHOETIC (CAVUM MEDULLARE)

COMPACT BONE SOLID CONTINOUS MASS, VERY DENCE LAMELLA SYSTEMOSTEON UNITE / HAVERS SYSTEM

MICROSTRUCTURE LAMELLA SYSTEMLAMELLA SIRCUFERENCIALLAMELLA INTERSTIRTIALLAMELLA CONCENTRIC (CYLINDERS) OSTEON UNITE / HAVERS SYSTEMCEMENTING LINEBONE MATRIX ORGANIC COMPONENT COLLEGENS FIBERS LAMELLAGROUND SUBSTANCEANORGANIC COMPONENT

COMPOSITION: CYLINDERS OF LAMELLAE (CONCENTRICCALLY), OSTEOCYTES IN LACUNAE HAVERSIAN CANAL (NEURO-VASCULAR IN CONNECTIVE TISUUE)LAMELLA CONCENTRIC; COLLAGEN TYPE I,. HELICAL ARRANGEMENT AROUND THE HAVERSIAN CANALTHIN CEMENTING LINEHAVERSIAN CANAL, OSTEOBLAST AND OSTEOPROGENITOR, (NEURO-VASCULAR IN CONNECTIVE TISUUE) OSTEONS HAVERSIAN UNIT

MICROSCOPIC STRUCTURE OF COMPACT BONEHAVERSIAN CANAL (CONNECTIVE TISSUE, VASCULAR, NERVE, LYMPH)CONCENTRIC LAMELLA ( COLLAGEN FIBERS)OSTEOCYTES IN LACUNAE, PROCESSUS IN INTERCELLULAR CANALICULITHIN CEMENTINTERSTITIAL LAMELLA

SPONGI/CANCELLOUS BONE POROUS BONE, BRANCHING BONY SPICULES/TRABECULAE, LABYRIN (BONE MARROW)

1. COLLAGENFIBERSCOLLAGEN I TYPE, (95%)HELICAL ARRANGEMENT AROUND THE HAVERSIAN CANAL

2. GROUND SUBSTANCE, MATRIX (ORGANIC) CALCIFIED ONLY 5%, IMPORTANT IN BONE METABOLISM AND MINERALIZATIONFILLS SPACE BETWEEN CELLS AND FIBERS, LUBRICANT & BARRIERMAINLY 2 CLASSES COMPONENT:1).GLYCOSAMINOGLICANS 2).STRUCTURAL GLYCOPROTEINSCALCIFIED, >> CALSIUM PHOSPHATE (CRYSTALS) HARDNESS OSEOMUCOID: (DURING OSTEOGENESIS) NONCALCIFIED

MATRIX OF BONE2. SPECIFIC BONE GLYCOPROTEIN (NONCOLLAGENUS PROTEIN, BONE OSTEOCALCIN, GLA PROTEIN, VIT K DEPENDENT (BINDS TO HYDROXYAPATITE),BONE SIALOPROTEIN, HAS BINDING SITES FOR MATRIX COMPONENTS AND INTEGRINS, (SUGESTING ITS INVOLVEMENT IN ADHERENCE OF THESE CELLS TO MATRIXS).OSTEOCALCIN AND SIALOPROTEIN, BOTH BIND CALCIUM AVIDLY AND MAY BE RESPONSIBLE FOR PROMOTING CALCIFICATION BONE MATRIXOSTEOPONTIN (ALSO BINDS TO HYDROXYAPATITE, BUT HAS ADDITIONAL BINDING SITE FOR OTHER COMPONENTS, FOR INTEGRINS (OSTEOBLASTS AND OSTEOCLASTS).BONE MORPHOGENIC PROTEINBONE PROTEOLIPIDBONE PHOSPHOPROTEINOSTEONECTINEBONE PROTEOGLYCANVITAMIN D STIMULATES THE SYNTHESIS OF THESE GLYCOPROTEINS

1. GLYCOSAMINOGLYCAN SULFAT GLYCOSAMINOGLYCANS (CHONDROITIN 4-SULFAT, CHONDROITIN 6-SULFAT, KERATAN SULFAT), WITH PAS REAGENT, SLIGHT METACHROMASIA NONSULFAT GLICOSAMINOGLICAN (HYALURONIC ACID, ONLY)

PROTEOGLYCAN: FORMATION AND COMPOSITION SULFATED GLYCOSAMINOGLICANS (CHONDROITIN SULFATE) WITH PROTEIN CORES FORM SMALL PROTEOGLYCAN MOLECULESLINGKING PROTEIN , BIND THE PROTEIN CORE TO THE LINEAR HYALURONIC ACID MOLECULES FORM VERY LARGE AGGRECAN COMPOSITES (AGGREGATED PROTEOGLYCANS MOLECULE).CHONDROITIN SULFAT , BIND TO COLLAGEN FIBERS FORMING CROSS-LINKED MATRIX.

CELLS OF BONE

CELLS OF BONE1) OSTEOPROGENITOR CELLS, (OSTEOGENIC) IN CELLULAR LAYER OF PERIOSTEUM 2) OSTEOBLAST, (SECRETE MATRIX), CELLULAR LAYER OF PERIOSTEUM, IN HAVERS CANALS3) OSTEOCYTES, (MATURE/INACTIVE), IN LACUNA , CALCIFIED MATRIX. 4) OSTEOCLAST, (RESORBS MATRIX , BONE RESORPTION AND REMODELING)

1. OSTEOPROGENITOR CELLS DRIVED EMBRYONIC MESSENCHYMAL CELLS, POTEN TO DIFFERENTIATE INTO OSTEOBLASTMOST ACTIVE DURING PERIOD BONE GROWTHDIFFERENTE INTO CHONDEROGENIC CELLS (UNDER LOW OXYGEN TENSION , REPAIR BONE) BECOME INTO OSTEOBLAST , UNDER INFLUENCE BONE MORPHOGENIC PROTEIN (BMP) FAMILY AND TRANSFORMING GROWTH FACTOR (TGF ) LOCATION : INNER CELLULAR LAYER OF PERIOSTEUM, LINNING HAVERSIAN CANAL , ENDOSTEUM . SPIDLE SHAPED, PALE STAINING OVAL NUCLEUS; PALE CYTOPLASMA, SPARSE RER, POORLY DEVELOPED GOLGI APPARATUS

Osteoprogentor cell: Stem cell whose divisions produce osteoblastLOCATION: ON SURFACE OF BONE IN PERIOSTEUM (CELLULAR LAYER), IN HAVERS CANALS (GROWTH BONE/REPAIR BONE)SYNTHESIZE ORGANIC MATRIXACTIVELY, BASOPHYLIC CYTOPLASMSECRETORY GRANULES (MATRIX PRECURSORS), PAS REAGEN VESICLES STAIN PINK.CYTOPLASM PROCESSES SHORT PROCESSES, NEIGHBORING OSTEOBLAST, LONG PROCESSES OSTEOCYT. FORM GAP-JUNCTIONS

intramembranous ossification OSTEOBLAST (Ob) line the bony spicule, secreting osteoid onto the bone. OSTEOCLAST (Oc), housed in Howship's lacunae.2. OSTEOBLASTS

Immature bone cell that secretes organic component of matrix 15CONTROLE OSTREOCLAST IN BONE RESORPTION (REMODELING,REPAIR BONE), SECRETEOSTEOPROTEGERIN LIGAND (OPGL), BY INTEGRIN & PTH STIMULATES SECRETE OPGLOPGL INDUCES DIFFERENSTIATION OF PREOSTEOCLATS , AND IT INCREASE RANKL EXRESSION. OSTEOCLAST-STIMULATING FACTOR (OSF) ACTIVATE OSTEOCLASTS TO RESORB BONEENZYMES REMOVING OSTEOID OSTEOCLASTS CAN MAKE CONTACT WITH MINERALIZED BONE SURFACESYNTHESE ORGANIC MATRIX (COLLAGEN I, PROTEOGLYCANS, GLYCOPROTEINS)

CLINICAL CORRELATIONS MONITOR BONE FORMATION

OSTEOBLAST CELLS MEMBRANES, >> ENZYME ALKALINE PHOSPHATASE. DURING ACTIVE BONE FORMATION, SECRETE HIGH LEVEL (ELEVATING LEVEL IN THE BLOOD).MONITOR BONE FORMATION (REPAIR BONE) MEASURING THE BLOOD ALKALINE PHOSPHATASE LEVEL.3. OSTEOCYTES IN LACUNA, NO CONTAC TO CALCIFIED MATRIX (OSTEOID BUMFER), MATURE-INACTIVE CELLS, (BUT SECRETE SUBSTANCES FOR BONE MAINTENANCE)PROCESSES IN CANALICULI GAP-JUNGTION TO NEIGBORING OSTEOCYTES AND OSTEOBLAST.EXTRACELLULAR FLUID NUTRIENS AND METABOLITSREMODELING: MECHANOTRANSDUCTION, STIMULATE TO RELEASING CYCLIC ADENOSINE MONOPHOSPHATE (cAMP), OSTEOCALCIN-LIKE GROWTH FACTOR , INSULIN-LIKE GROWTH FACTOR, FACILITATES THE REQRUITMENT OF PREOSTEOBLAST TO ASSIST IN THE REMODELING OF SKELETON

Osteocytes trapped in calcified matrix, in lacunaRESORBING BONE DIE (APOPTOSIS). (GROWTH, REMODWLING, REPAIR BONE)RECEPTOR :OSTEOCLAST-STIMULATING FACTOR (OSTEOBLAST) AVCTIVE RESORBOSTEOPROTEGERIN (OPG) (OSTEOBLAST)CALCITONIN. (OSTEOBLAST) BONE MINERALISASIMACROPHAGE COLONY-STIMULATING FACTOR-1,LARGE, MOTILE, MULTINUCLEATED , ACIDOPHILIC CYTOPLASM. DERIVED FROM FUSION OF MANY BLOOD-DRIVED MONOCYTES, PRECUSOR ORIGINATES IN BONE MARROW, OSTEOCLAST PRECUSORS FUSE, MULTINUCEATED OSTEOCLAST,

intramembranous ossificationOsteoclasts (Oc) in Howship's lacunae.4. OSTEOCLAST

Multinucleate cell, secretes acid and enzym to dissolve bone matrix19DENSE, IRREGULAR, COLLAGENOUS CONNECTIVE TISSUE,OUTER FIBROUS LAYER, (VASCULAR AND NERVE) SUPPLY O2 & NUTRISIEN INNER CELLULAR LAYER (OSTEOPROGENITOR & OSTEOBLASTS). OSTEOGENESIS, REMODELING, RECOVERY FRACTURE

PERIOSTEUM-ENDOSTEUM

CIRCUMFERENTIAL EXTERNAL-INTERNAL, CONCENTRIC (OSTEON UNIT), INTERSTITIAL LEMELLAE.

UNIT OSTEON, HAVERS SYSTEMLAMELLA CONCENTRICCEMENTHAVERS CANALOSTOCYTES, LACUNA, CANALICULISYSTEM OF LAMELLAESYSTEM OF VASCULAR-CANALPERIOSTEAL BLOOD VESSELPERFORATING (VOLKMAN ,S CANAL)HAVERSIAN CANALCONTINUOUS INTO MEDULLARY CAVITYCANALICULI, LACUNA SPACE (EXTRACELLULAR FLUID)

SYSTEM OF VASCULAR-CANAL - NUTRIEN & GASS TRANPORTATION

EXTRACELLULAR FLUID (PERIOSTEOCYTIC SPACE, CANALICULI), EXTENSIVE NETWORK OF CANALICULI AND OF PERIOSTEL SPACE VOLUME (1,3L), AND AREA OF WALLS EXCHANGES (5000 m2) , 20 g CALCIUM CAN RESOBED ACCESS TO BLOODS TREAM ENSURES THE MAINTENANCE OF ADEQUATE BLOOD CALCIUM LEVELS.

BONE RESORPTIONBONE RESORPTIONOBJECTIVEIMPORTANT OSTEOCLAST FUNCTION :GROWTH AND DEVELOPMENT OF BONE OSTEOGENESIS REPAIR OF DAMAGE/FRACTUREPHYSIOLOGY OF THE SCELETON.HOMEOSTASIS MAINTENANCE Ca BLOOD LEVEL REMODELING RENEWING BONE TISSUEPHATOPHYSIOLOGY OF SEVERAL SCELETAL DISEASE BONE RESORPTION RATE INCREASED (OSTEOPOROSIS, METATASTIC BONE DISEASE AND PAGETS DISEASE OF BONE) DECREASE (VARIUOS SYNDROME OF OSTEOPETROSIS)

BONE RESORPTIONLOW Ph ENVIRONMENT INORGANIC MATRIX IS DISOLVED, (Ca) OSTEOCLAST CYTOPLASM , BE DELIVERED TO NERLY CALILLARIES.SYNTHESE LYSOSOMAL ENZYM, SECRESE TO APICAL RUFFLED BORDER MEMBRANE ACIDOPILIC MILIEUMECHANISM OF OSTEOCLAST TO BONE RESORPTION

FORMATION OF CARBONIC ACID , ENZYME CARBONIC ANHYDRASE CATALYSES: CO2 + H2O H2CO3, H+ & HCO3PROTON PUMPS IN (RUFFED BORDER) ACTIVELY TRANSPORT H+ IONS SUBOSTEOCLASTIC COMPARTEMENT LOW pH OF MICROENVIRONMENT

REGULATE THE NUMBER OF OSTEOCLAST

VIA PRECUSSOR OSTEOCLAST, STIMULATE/INHIBITE PROLIFERATION AND DIFFERENTIATION (OSTEOPROGENITOR, OSTEOBLAST, MACROPHAGE, OTHERS)VIA OSTEOBLAST , INHIBITE TO PRODUCTING FACTOR THAT ESSENTALE FOR OSTEOCLAST DIFFERENSIATION (CALSITONIN AND AMINOBIPHAPHONATE), VIA DIRECT TO OSTEOCLAST, INDUCE APOPTOSIS CELLS ((BISPHOSPHONATE, CLODRONATE)VIA THE RANK/RNKL/OSTEOPROGETERIN PATHWAYREGULATION OF BONE RESORPTION (BONE LOSS)1. LOCAL FACTORS (PRODUCED IN THE BONE MICROENVIRONMENT)

RANKL (+) (RECEPTOR ACTIVATOR OF NUCLEAR FAKTOR KAPPA B LIGAND/NF-KB) PRODUCED BY BONE CELLS (OSTEOBLASTIC LINEARGE CELL & ACTIVATED T LYMPHOCYTERECEPTOR : ON OSTEOCLASTIC PRECUSOR , MACROPHAGE, STROMA CELL, OSTEOBLASTFOR OSTEOCLAST FORMATION/DIFFERENTIATION INTO MULTINUCLEATED OSTC, FUSSION, ACTIVATION & SURVIVAL INCREASE NUMBER & ACTIVATING OF OSTEOCLAST,

EFFECT OF RNAK CONTRACTED, BY COUNTERACTED BY OPG (ACTS SOLUBLE NETRALIZING RECEPTOR)RANKL & OPG ARE REGULATED BY VARIANS HORMON (GLUCOCORTICOID, PTH, CALCITONIS, VIT D GROWTH HORMON, TESTOSTERO, ESTROGENABNORMALITIES OF RANK/OPG SYATEM IMPLICATED IN THE PATOGENIS OF POSTMENOPAUSE OSTEOPOROSIS, RHEUMATID ARTRITIS, PAGET,S DIS. PERIODONTAL DIS, ETC

OPG (OSTEOPROGERIN) (-) = OSTEOCLAST GENESIS INHIBITORY FACTOR (OCIF), A MEMBER OF THE TUMOR NECROSIS FARTOR RECEPTOR (TNFR) FAMILY,PRODUCED BY OSTEOBLASTRECEPTOR : ON OSTEOCLASTIC PRECUSOR, MACROPHAGE, STROMA CELL, OSTEOBLASTOPG RECEPTOR FOR RANKL PREVENTING BINDING TO RANK, INHIBITOR OF RANKL, BLOCKS THE EFFEK OF RANKL INHIBITS OSTEOCLAST DIFFERENTIATION

RANKL, CELLULAR RECEPTOR RANK, & DECOY RESEPTOR OPG, CONSTITUTE NOVEL CYTOKINE SYSTEM. REGULATES OSTEOCLASTIC ACTIVITY MAINTAINING A CONSTAN SUPPLY CALCIUM ION. SYSTEMIC FACTORS, HORMONAL EFFECTS.1. PTH; PARENCHYMAL CELLS (PARATHYROID GLAND) SENSITIVE TO BLOOD CALCIUM LEVEL FALL BELOW NORMAL, INCREASE Ca RECEPTOR : VIA OSTEOBLAST TO OSTEOCLAST (LACK PTH RECEPTOR)

PTH ACTIVATES RECEPTOR ON OSTEBLAST, SUPPRESSING MATRIX FORMATION AND INITIATING MANUFACTURE AND SECRETION OF OPGL & OSTEOCLAST-STIMULATING FACTOR INDUCE OSTECLAST FORMATION AND STIMULATE QUIESCENT OSTEOCLAST (BECOM ACTIVE), RELEASE OF CALCIUM ION. PTH SLIGHT INCREASED EXPRESSION OF IL-6 mRNA IN PRIMARY OSTEOBLAST-LIKE CELLS INDUCES BONE RESOPTION

292. CALCITONIN (CT):THYROID GLD, PARAFOLLICULAR CELLS (C cells) CALCIUM ION LEVEL IN PLASMA ELEVATED SECRETE CALCITONIN,RECEPTOR ON OSTEOBLASTIMPORTAN ROLES IN Ca HOMEOSTASIS DECREASE Ca ACTIVATES RECEPTOR ON OSTEOCLASTS, INHIBITE RESORBING BONE. STIMULATE OSTEOBLASTS TO INCREASE OSTEOID SYNTHESIS AND CALCIUM DEPOSITION IS INCREASE.3. GROWTH HORMON SOMATOTROPIN (ANT. LOBE OF PITUITARY GLAND), BONE DEVELOPMENT VIA SOMATOMEDINS (insulin-like growth factors), ESPECIALLY STIMULATING GROWTH OF THE EPIPHYSEAL PLATE.CHILDREN DEFICIENT THIS HORMONE DWARFISM, EXCESS SOMATOTROPIN IN THEIR GROWING YEARS PIPTUTARY GIGANTISM.

REGGULATION OF DIFFERENTIATION OSTEOCLAST

OSTEOBLASTS , SECRETE 3 SIGNALING MOLECULES REGULATE THE DIFFERENTIATION OF OSTEOCLASTS.SECRETE OSTEOCLAST-STIMULATING FACTOR ACTIVATE OSTEOCLASTS TO RESORB BONESECRETE ENZYMES REMOVING OSTEOID OSTEOCLASTS CAN MAKE CONTACT WITH MINERALIZED BONE SURFACEOPG, (IS PRODUCED NOT ONLY BY OSTEOBLAST), BY CELLS OTHER TISSUE (CARDIOVASCULAR SYSTEM, LUNG, KIDNEY, ISTESTINES, HEMAPOETIC AND IMMUNE CELLS).IN BONE, OPG ALSO SUPRESSES THE OSTEOCLASTS BONE RESOPTIVE CAVITIES. (NOT ONLY INHIBITS THE DIFFERENTIATION OF PRECUSOR CELLS INTO OSTEOCLAST)REMODELING OF BONEREMODELLING of BONE

OsteoclastHowships lacunaPHYSIOLOGICAL , CONTINOUS RENEWING BONE DURING LIFELONGMATUR BONE TISSUE IS REMOVED (BONE RESORPTION) AND NEW BONE TISSUE IS FORMATED (OSSIFICATION), CONTINOUS TURNOVER OF BONE TO MAINTENANCE NORMAL BONE MASS. DEFINITION:

REMODELING FUNGTIONAL, ADAPTATION WITHIN THE SCELETON, ACTIVE AND DYNAMIC PROCESS CORRECT BALANCE BETWEEN BONE FORMATION /DEPOSITION AND BONE RESORPTION, IN YOUNG PERSON, BONE DEVELOPMENT EXCEES RESORPTION ,IN ADULTHOOD, EPIPHYSEAL PLATES CLOSE AND BONE GROWTH HAS BEEN ATTAINED, NEW BONE DEVELOPMENT IS BALANCED WITH BONE RESORPTION.CONTINUING REMODELING TO MEET STRESSES PLACED ON IT.

PHYSIOLOGICAL PROCESS, NECESSARY FOR:

TO HEMOSTASIS CALCIUM (CALCIUM METABOLIC)TO REORGANITATION OR RENOVATION OF OLD STRUCTURE OF BONE (RENEWING BONE TISSUE)TO MAINTENANCE NORMAL BONE MASS,(HELATHY BONE), TO ENSURE MAINTENNCE OF NORMAL BONE MASS AS PERSONE AGES FISRT YEARS OF LIFE , 100% OF THE SCELETON IS REPLACE, IN ADULT 10%/YEARTO CONTROLE THE RESHAPING OR REPLACEMENT OF BONE FOLLOWING:INJURY (FRACTURE) OR MICRODAMAGE WHICH ACCOR DURING NORMAL ACTIVITYMECANICAL STRESSING OF PHYSISC OCCUR IN BONE, STRUCTUR SUPPORT

OBJECTIVE PROCESS OF REMODELINGBONE REMODELING, 3 PHASES RESORPTION MATRIX : OSTEOCLAST OSTEOCLAST BREAK DOWN BONE AND RELEASE THE MINERAL (RESORPTION OF BONE)REVERSAL : MONONUCLEAR CELLS APPEARS ON BONE SURFACEFORMATION NEW BONE : OSTEOBLASTS, LAY DOWN NEW BONE REPLACED RESORBED BONE COMPLITELYACTIVATION OF OSTEOCYTS, OSTEOBLAST, OSTEOCLASTS ARE REGULATED BY PRAHORMON AND HORMON (PTH, CALCITONIN, TESTOSTERON, ESTROGEN, VIT D. )

HISTOGENESIS OF BONE1. INTRAMEMBRANOUS BONE FORMATION/OSSIFICATION2. ENDOCHONDRAL ONE FORMATION/OSSIFICATION

HISTOGENESIS OF BONE

BONE FORMATION (OSSIFICATION) DURING EMBRYONIC DEVELOPMENT & REPAIR OF FRACTURE BONE FIRS BORNE FORMED, PRIMARY BONE (IN GROW), AND LATER RESORBED AND REPLACED BY SCONDARY BONE. (MATURE BONE)SECONDARY BONE CONTINUES TO BE RESORBED THROUGHOUT LIFE, ALTHOUGH AT SLOWER RATE. (REMODELING)

PROCESS INTRAMEMBRANOUS OSSIFICATION (PLATE BONE)WITHIN MESSECHYMAL TISSUE (PRIMARY OSSIFICATION CENTER)

MESSENCHYMAL CELLS FORM AGRGREAGATION DIFFERENTITE INTO OSTEOBLASTS BONE MATRIX (OSTEOID)OSTEOBLASTS POPULATION ON SURFACE BONE GROW IN LINEAR EXTENSIONS (SPICULES). A NETWORK OF TRABECULAE CALCIFICATION QUICKLY FOLLOWS OSTEOID FORMATION, OSTEOBLAST TRAPPED IN BONE MATRICES, OSTEOCYTES, IN LACUNA AND A SYSTEM OF CANALICULI.MULTIPLE OSSIFICATION CENTERS , ENLARGE FUSION OF SPICULES IN THE TRABECULAR NETWORK (CHARATERISTC OF SPONGY BONE). REMODELING, PRODUCES SPONGY BONE, MARROW CAVITIES AND COMPACT BONE CHARASTERITIC OF MATURE BONE.,

ADDITION OF TRABECULAE INCREASE THE SIZE LARGE BONE, (OCCIPATLE), HAVE SEVERAL OSSIFICATION CENTER, FUSE TO FORM SINGLE BONE.REMAIN REGIONS OF MESSENCHYMAL TISSUE UNCALCIFIED DIFFERENTIATED INTO THE PERIOSTEUM AND ENDOSTEUM OF DEVELOPING BONE.

REQUIRES THE PRESENCE OF CARTILAGE TEMPLATE (HYALINE)SEVERAL PHASE PROCESS FORMATION & GROWTH OF HYALIN CARTILAGE MODEL, PRIMARY OSSIFICATION CENTERSECONDARY OSSIFICATION CENTERBONE GROWTH IN LENGTH AND GROWTH IN WIDTH REMODELING ENDOCHONDRAL BONE FORMATIONIN LONG AND SHORT BONES

HYALINE CARTILAGE MODEL GROWS (INTERSTITIEL & APOSITIONAL)CARTILAGE AT MIDRIFF (DIAPHYSIS) IS INVADED BY VASCULARIN THE CENTER OF DIAPHYSIES, CHONDROCYTES HYPERTHROPY, MATRIX BEGIN TO CALCIFIED DEFICIT NUTRIENTS DIE, LEAVING CAVITIES, WITHIN THE CALCIFIED CARTILAGE MATRPERICHONDRIUM TRANSFORM INTO PERIOSTEUM (OSTEOGENIC LAYER). OSTEOCLAST INVADE, ETCH BONE TO PERMiT PERIOSTEAL BUD TO FORM, CAPILLARIES, OSTEOPROGENITOR CELLS PERIOSTEUM MIGRATE INTO , OSTEOBLASTS REPLACE PRODUCES SPONGY BONE. BECOMES PRIMARY OSSIFICATION CENTER IN DIAPHYSES. A SUBPERIOSTEAL THIN BONY COLLAR ARROUND THE SHAFT OF CARTILAGE MODEL. , EPIPHYSES BECOME FILLED WITH SPONGY BONE. A THIN CAP OF CARTILAGE REMAINS (ARTICULAR CARTILAGE), METHAPHYSEAL PLATE SPARATES THE EPIPHYSES FROM DIAPHYSIS.CENTER OF DIAPHYSES NOW BEGIN TO CALCIFIED, CAPILLARES AND OSTEOBLAST MIGRATE TO THESE AREA CREATING SECUNDARY OSSIFICATION CENTER.SCUNDARY OSSIFICATION CENTER APPEAR IN THE EPIPHYSES, SIMILAR TO THAT DISCRIBED ABOVE FAR THE PRIMARY OSSIFICATION CENTER, PROCESS OF ENDOCHONDRAL FORMATION/OSSIFICATION

Endochondral bone formation (14). The upper half; cartilage (C) containing chondrocytes mature, hypertrophy, and calcify at the interface (matrix); The lower half : calcified cartilage/bone complex (arrows) is being resorbed and bone (b) is being formed. P, periosteum.

Endochondral bone formation (270). The trabeculae of calcified cartilage (CC) are covered by a thin layer of bone (darker red) with osteocytes embedded in it (arrows) and with osteoblasts (Ob) lying next to the boneTHE CONTINUED LENGTHENING OF BON DEPENDS ON THE EPIPHYSEAL PLATE.EPIPHYSEOUS FILLED WITH SPONGY BONE, THIN HYALIN CARTILAGE REMAIN ARTICULAR SURFACE (ARTICULAR CARTILAGE). EPIPHYSEAL PLATE : CHONDROCYTES PROLIFERATE, THE PROCESS OF ENDOCHONDRAL BONE FORMATION. (PROLIFERATION AT EPIPHYSEAL ASPECT, REPLACEMENT BY BONE AT THE DIAPHYSEAL SIDE (TAKES PLACE).THE EPIPHYSEAL PLATE SPARATE THE BONE OF THE EPIPHYSES FROM DIAPHYSIS. GROWTH IN THE LENGTH

BONE GROWTH IN LENGTH

EPIPHYSEAL PLATE IS DIVIDED INTO 5 ZONE1). ZONE OF RESERVE CARTILAGO: CHONDRCYTES RANDOMLY DISTRIBUTED, MITOCALLY ACTIVE. 2). ZONE OF PROLIFERATION: CHONDROCYTES RAPIDLY PROLIFERATING, FORM ROWS OF ISOGENOUS CELLS THAT PARALLEL DIRECTION OF BONE GROWTH. 3). ZONE OF MATURATION & HYPERTROPHY : CHONDROCYTES HYPERTROPHY, ACCUMULATE GLYCOGEN , LACUNA >, MATRIX BETWEEN LACUNAE NARROW.4). ZONA OF CALCIFICATION : LACUNAE BECOME CONFLUENT, HYPERTROPHIED CHONDROCYTES DIE, MATRIX CALCIFIED. 5). ZONE OF OSSIFICATION: OSTOEPROGENITOR CELLS INVADE THE AREA, DIFFERENTIATE INTO OSTEOBLASTS, MATRIX CALCIFIED (ON THE SURFACE OF CALCIFIELD CARTILAGE). FOLLOW RESORPT THE CALCIFIED CARTILAGE/CALCIFIED BONE COMPLEX.

BY APPOSITIONAL GROWTH REPLACED BY BONE (BONE LENGTHENING BY PROLIFERATION AND INTERSTITIAL GROWTH OF CARTILAGO,.OSTEOPROGENITOR CELLS (PERIOSTEUM) INTO OSTEOBLAST SUBPERIOSTEAL BONE SURFACE.CINTINUOUSLY THROUGHT THE TOTAL PERIODE OF BONE GROWTH AND DEVELOPMENT, DURING BONE GROWTH AND DEVELOPMENT, RESORPTION IS AS IMPORTANS AS DEPOSISITION. FORMATION OF BONE ON THE OUTSIDE, MUST BE ACCOMPANIED BY OSTEOCLASTIC ACTIVITY INTERNALLY THE MARROW SPACE BE ENLARGED.BONE GROWTH IN WIDTH REPAIR OF BONE FRACTUREREPAIR OF BONE FRACTUREFRACTURE DAMAGE OF TISSUEBREAK OF VASCULLARBLEEDING CLOTING BLOOD BONE CELLS WILL DIE (NO NUTRITION) AND AREA WILL BECOME IRRITATED.4 STEPS TO REPAIR OF BONE FRACTURE

4 STEPS TO REPAIR OF BONE FRACTUREHEMATOMA -BLOOD VESSEL, BONE CELL WITH NO NUTRITION WILL DIE AND AREA WILL BECOME IRRITATED.. FIBROCARTILAGINOUS CALLUS (SOFT CALLUS) FORMATION. INVADE FIBROBLAST AND HYPERVASCULARITATION FORM GRANULATIONDEVELOPING BLOOD VESSELS, AND FIBROCARTILAGE FORMSBONE CALLUS (HARD CALLUS) FORMATION, ABOUT 1 WEEK NEW BONE BEGIN TO REPAIR (A BONY CALLUS) 3 MONTHS BONY CALLUS REPLACE THE FIBROCARTILAGE BONE REMODELING,

INITIAL EVENTS INVOLVED IN FRACTURE HEALING OF LONG BONE. PERIOSTEUM IS TORN OPPOSITE THE SPOT OF IMPACTAND, IN MANY INSTANCE, IS INTACT ON OTHER SIDEAN ACCUMULATION OF HEMATOMA BENEATH THE PERIOSTEUM AND BETWEEN THE FRACTURE ENDNECROTIC MARROW AND DEAD BONE CLOSE TO THE FRACTURE LNE

EARLY REPAIR. THERE IS ORGANIZATION OF HEMATOMA, EARLY PRIMARY NEW BONE FORMATION IN SUBPERIOSTEAL REGION, AND CARTILAGE FORMATION IN OTHER AREAS.

AT LATER STAGE IN THEREPAIR, EARLY IMMATURE FIBER BONE IS BRIDGING THE FRACTURE GAPPERSISTENT CARTILAGE IS SEEN AT POINTS MOST DISTANT FROM INGROWING CAPILLARY BUSDIN MANY INSTANCES, THESE ARE SUROUNDED BY YOUNG NEW BONE.IF FRAGMENTS OF BONE ARE LOST, OR DAMAGED SO SEVERELY THAT THEY HAVE TO BE REMOVE, "bony union" IS NOT POSIBLEPROCESS BONE REPAIR CANNOT ACCUR (BONY CALLUS DOES NOT FORM).IN THIS CASES, A BORNE GRAFT IS REQUIREDAUTOGRAFTS MOST SUCCESFUL BECOUSE RECIPIENT IS DONOR. HOMOGRAFTS DONOR FROM DOFFERENT INDIVIDUAL, MAY BE REJECTED (IMMUNOLOGICAL RESPONS)HETEROGRAFTS, GRAFTS FROM DIFFERENT SPECIES, LEAST SUCCESSFUL, ALTHOUGH CALFT BONE LOSES SOME OF ITS ANTIGENICITY WORTHY BONE GRAFT WHEN NECESSARY.CLINICAL CORRELATIONS Bone deseasesBONE DISEASESDue to inadequate osteoide.g., Vitamin CScurvy Due to inadequate mineralizatione.g., Ca++, PO4, Vitamin Drickets osteomalacia Due to excessive resorptionEndocrinopathiese.g., osteoporosis

CLINICAL CORRELATIONS ACROMEGALY.

ADULT WHO PRODUCE AN EXCESS OF SOMATOTROPIN, ABNORMAL INCREASE IN BONE DEPOSITION (WITHOUT NORMAL BONE RESORPTION). THICKENING OF THE BONES, ESPECIALLY OF FACE, CLOSURE OF THE EPIPHYSEAL PLATE IS NORMALLY RATHER STABLE AND CONSTANT ( >> SEXUAL MATURATION).PRECOCIOUS SEXUAL MATURATION STUNT SKELETAL DEVELOPMENT EPIPHYSEAL PLATE CLOSE TOO EARLY.SEXUAL MATURATION IS RETARDED, SKELETAL GROWTH CONTINUES BEYOND NORMAL LIMITS EPIPHYSEAL PLATE NOT CLOSE.CLINICAL CORRELATIONS OSTEOPOROSIS

DECREASING OF BONE MASSCHRONICALLY IMMOBILIZED, >> WOMEN OLDER 40, ESPECIALLY POSTMENOPAUSAL WOMEN, MORE SERIOUS AFTER MENOPAUSE, (ESTROGEN SECRETION DROPS). OFTENBINDING ESTROGEN TO SPECIFIC RECEPTOR ON OSTEOBLASTS ACTIVES TO MANUFACTURE AND SECRETE BONE MATRIX.DIMINISHED ESTROGEN, OSTEOCLASTIC ACTIVITY IS GREATER THAN BON DEPOSITION, REDUCTING BONE MASSESTROGEN REPLACEMENT (+). BUT INCREASE THE RISK.EARLY DIAGNOSTICNUTRITIONAL EFFECTS (IN NORMAL GROWTH)NORMAL BONE GROWTH IS SENSITIVE AND DEPENDENT ON SEVERAL FACTORS.PROTEIN, MINERAL, AND VITAMINS, THE AMNOACIDS ESSENTIAL FOR COLLAGEN SYNTHESSIS (BY OSTEOBLASTS).CALCIUM AND PHOSPHORUS CALCIFIED MATRIX VIT. D, CALCIUM ABSORBTION FROM INTESTINE (RICKETSIA IN CHILDREN)VIT. A & C, NECESSARY FOR PROPER SKELETAL DEVELOPMENT(SCURVY)OSTEOMALACIA= ADULT RICKETSPROLONGED DEFICIENCY VITAMIN D.NEWLY FORMED BONE IN PROCESS OF REMODELING DOES NOT CALCIFIED.MAY BECOME SEVERE DURING PREGNANCY BECAUSE THE FETUS REQUIRES CALCIUM, WHICH MUST BE SUPPLIED BY THE MOTHER.SCURVY.DEFICIENCY OF VITAMIN C.DEFICIENT COLLAGEN PRODUCTION, REDUCTION IN FORMATION OF BONE MATRIX AND BONE DEVELOPMENT.HEALING IS DELAYEDRICKETS DISEASE IN INFANTS AND CHILDREN, DEFICIENT IN VIT D. THE INTESTINEAL MUCOSA CANNOT ABSORB CALCIUM DISTURBANCES IN OSSIFICATION OF THE EPIPHYSEAL TO POORLY CALCIFIED BONE MATRIX.DEFORMED BONE PARTICULARLY IN THE LEGS, BECAUSE THE BONE CANNOT BEAR THEIR WEIGHT.JOINT

1) SYNARTHROSES. ONLY MINIMUM MOVEMENT, 2, DIARTHROSES FREE TO ARRTICULAE , WIDE RANGE OF MOTION SYNARTHROSIS JOINT: 3 TYPES, (TISSUE MAKING UP THE UNION) 1) SYNOSTOSIS, JOINT UNITING TISSUE IS BONE (e.g., SKULL BONE IN ADULT), 2) SYNCHONDROSIS, JOINT UNITING TISSUE IS HYLANIN CARTILAGE (e.g., JOINT OF FIRST RIB STERNUM), 3) SYNDESMOSIS, BONES ARE JOINED BY DENCE CONNECTIVE TISSUE (e.g., PUBIC SYMPHYSIS). LONG BONE, DIARTHROSIS (MOST JOINTS OF EXTREMITIES). ARTICULAR SURFACE, HYALIN CARTILAGE (ARTICULAR GARTILAGE). LIGAMNETS MAINTEN THE CONTACT BETWEEN BONES.JOINT CAPSULE : 1). OUTHER FIBROUS LAYER CONNECTIVE TISSUE CONTINOUS WITH PERIOSTEUM, 2) INNER CELLULAR SYNOVIAL LAYER,(SYNOVIAL MEMBRANE), COVER ALL NONARTICULAR SURFACE. BONE ARTICULATE , SYNOVIAL FLUIDHIGH CONCENTRATION OF HYALURONIC ACID AND GLYCOPROTEIN LUBRICIN COMBINE WITH FILTRATE OF PLASMA.TO SUPPLYING NUTRIENS AND OXYGEN TO CHONDROCYTES OF ARTICULAR CARTILAGE, TO LUBRICANT FOR JOINT (HIGH CONTEN HYALURONIC ACID AND LUBRICIN).MACROPHAGE IN SYNOVIAL FLUID ACT TO PHAGOCYTOSES DEBRIS IN JOINT SPACE. TYPE CELLS IN SYNOVIAL LAYER : 1). TYPE A CELLS ARE MACROPHAGES PHAGOCYTIC CELLS RESPONSIBLE FOR REMOVING DEBRIS FROM JOINT SPACE. 2). TYPE B CELLS RESEMBLE FIBROBLAST, TO SECRETE THE SYNOVIAL FLUID.

DOKTER ADALAH PILIHANKU PROSES ADALAH IKHTIAR DAN PENGKODISIANKURIDHO ALLAH DOAKUSUKSES UNTUK MU,AMIIIIN.