Y khoa, y dược - Bones and skeletal tissues: Part B

6 Bones and Skeletal Tissues: Part BBone DevelopmentOsteogenesis (ossification)—bone tissue formationStagesBone formation—begins in the 2nd month of developmentPostnatal bone growth—until early adulthoodBone remodeling and repair—lifelongTwo Types of OssificationIntramembranous ossificationMembrane bone develops from fibrous membraneForms flat bones, e.g. clavicles and cranial bonesEndochondral ossificationCartilage (endochondral) bone forms by replacing hyaline cartilageForms most of the rest of the skeletonFigure 6.8, (1 of 4)MesenchymalcellCollagenfiberOssificationcenterOsteoidOsteoblast Ossification centers appear in the fibrousconnective tissue membrane.• Selected centrally located mesenchymal cells cluster and differentiate into osteoblasts, forming an ossification center.1Figure 6.8, (2 of 4)OsteoidOsteocyteNewly calcifiedbone matrixOsteoblast Bone matrix (osteoid) is secreted within thefibrous membrane and calcifies.• Osteoblasts begin to secrete osteoid, which is calcified within a few days.• Trapped osteoblasts become osteocytes.2Figure 6.8, (3 of 4)Mesenchymecondensingto form theperiosteumBlood vesselTrabeculae ofwoven bone Woven bone and periosteum form.• Accumulating osteoid is laid down between embryonic blood vessels in a random manner. The result is a network (instead of lamellae) of trabeculae called woven bone.• Vascularized mesenchyme condenses on the external face of the woven bone and becomes the periosteum.3Figure 6.8, (4 of 4)FibrousperiosteumOsteoblastPlate ofcompact boneDiploë (spongybone) cavitiescontain redmarrow Lamellar bone replaces woven bone, just deep tothe periosteum. Red marrow appears.• Trabeculae just deep to the periosteum thicken, and are later replaced with mature lamellar bone, forming compact bone plates.• Spongy bone (diploë), consisting of distinct trabeculae, per- sists internally and its vascular tissue becomes red marrow.4Endochondral OssificationUses hyaline cartilage models Requires breakdown of hyaline cartilage prior to ossificationFigure 6.9 Bone collarforms aroundhyaline cartilagemodel. Cartilage in thecenter of thediaphysis calcifiesand then developscavities. The periostealbud inavades theinternal cavitiesand spongy bonebegins to form. The diaphysis elongatesand a medullary cavityforms as ossificationcontinues. Secondaryossification centers appearin the epiphyses inpreparation for stage 5. The epiphysesossify. Whencompleted, hyalinecartilage remains onlyin the epiphysealplates and articularcartilages.HyalinecartilageArea ofdeterioratingcartilage matrixEpiphysealblood vesselSpongyboneformationEpiphysealplatecartilageSecondaryossificationcenterBloodvessel ofperiostealbudMedullarycavityArticularcartilageChildhood toadolescenceBirthWeek 9Month 3SpongyboneBonecollarPrimaryossificationcenter12345Figure 6.9, step 1 Bone collar forms aroundhyaline cartilage model.1Hyaline cartilageWeek 9Bone collarPrimaryossificationcenterFigure 6.9, step 2 Cartilage in the centerof the diaphysis calcifiesand then develops cavities.2Area of deterioratingcartilage matrixFigure 6.9, step 3 The periosteal bud inavadesthe internal cavities andspongy bone begins to form.3SpongyboneformationBloodvessel ofperiostealbudMonth 3Figure 6.9, step 4 The diaphysis elongates and a medullary cavity formsas ossification continues. Secondary ossification centersappear in the epiphyses in preparation for stage 5.4Epiphysealblood vesselSecondaryossificationcenterMedullarycavityBirthFigure 6.9, step 5 The epiphyses ossify. When completed, hyaline cartilageremains only in the epiphyseal plates and articular cartilages.5Epiphyseal platecartilageArticular cartilageChildhood to adolescenceSpongy boneFigure 6.9 Bone collarforms aroundhyaline cartilagemodel. Cartilage in thecenter of thediaphysis calcifiesand then developscavities. The periostealbud inavades theinternal cavitiesand spongy bonebegins to form. The diaphysis elongatesand a medullary cavityforms as ossificationcontinues. Secondaryossification centers appearin the epiphyses inpreparation for stage 5. The epiphysesossify. Whencompleted, hyalinecartilage remains onlyin the epiphysealplates and articularcartilages.HyalinecartilageArea ofdeterioratingcartilage matrixEpiphysealblood vesselSpongyboneformationEpiphysealplatecartilageSecondaryossificationcenterBloodvessel ofperiostealbudMedullarycavityArticularcartilageChildhood toadolescenceBirthWeek 9Month 3SpongyboneBonecollarPrimaryossificationcenter12345Postnatal Bone GrowthInterstitial growth:  length of long bonesAppositional growth:  thickness and remodeling of all bones by osteoblasts and osteoclasts on bone surfacesGrowth in Length of Long Bones Epiphyseal plate cartilage organizes into four important functional zones: Proliferation (growth)HypertrophicCalcificationOssification (osteogenic)Figure 6.10Calcified cartilagespiculeOsseous tissue(bone) coveringcartilage spiculesResting zoneOsteoblast depositingbone matrix Proliferation zoneCartilage cells undergo mitosis. Hypertrophic zoneOlder cartilage cells enlarge. Ossification zoneNew bone formation is occurring. Calcification zoneMatrix becomes calcified; cartilage cells die; matrix begins deteriorating.1234Hormonal Regulation of Bone GrowthGrowth hormone stimulates epiphyseal plate activityThyroid hormone modulates activity of growth hormoneTestosterone and estrogens (at puberty)Promote adolescent growth spurtsEnd growth by inducing epiphyseal plate closureFigure 6.11Bone growthBone remodelingArticular cartilageEpiphyseal plateCartilagegrows here. Cartilageis replacedby bone here.Cartilagegrows here. Bone isresorbed here. Bone isresorbed here. Bone is addedby appositionalgrowth here. Cartilageis replacedby bone here.Bone DepositOccurs where bone is injured or added strength is neededRequires a diet rich in protein; vitamins C, D, and A; calcium; phosphorus; magnesium; and manganeseBone DepositSites of new matrix deposit are revealedby theOsteoid seamUnmineralized band of matrixCalcification frontThe abrupt transition zone between the osteoid seam and the older mineralized boneBone ResorptionOsteoclasts secreteLysosomal enzymes (digest organic matrix)Acids (convert calcium salts into soluble forms)Dissolved matrix is transcytosed across osteoclast, enters interstitial fluid and then bloodControl of RemodelingWhat controls continual remodeling of bone?Hormonal mechanisms that maintain calcium homeostasis in the bloodMechanical and gravitational forces Hormonal Control of Blood Ca2+Calcium is necessary forTransmission of nerve impulsesMuscle contractionBlood coagulationSecretion by glands and nerve cellsCell divisionHormonal Control of Blood Ca2+Primarily controlled by parathyroid hormone (PTH) Blood Ca2+ levels Parathyroid glands release PTHPTH stimulates osteoclasts to degrade bone matrix and release Ca2+  Blood Ca2+ levels Figure 6.12Osteoclastsdegrade bonematrix and release Ca2+into blood.ParathyroidglandsThyroidglandParathyroidglands releaseparathyroidhormone (PTH).StimulusFalling bloodCa2+ levelsPTHCalcium homeostasis of blood: 9–11 mg/100 mlBALANCEBALANCEHormonal Control of Blood Ca2+May be affected to a lesser extent by calcitonin Blood Ca2+ levelsParafollicular cells of thyroid release calcitoninOsteoblasts deposit calcium salts  Blood Ca2+ levelsLeptin has also been shown to influence bone density by inhibiting osteoblastsResponse to Mechanical StressWolff’s law: A bone grows or remodels in response to forces or demands placed upon itObservations supporting Wolff’s law:Handedness (right or left handed) results in bone of one upper limb being thicker and strongerCurved bones are thickest where they are most likely to buckleTrabeculae form along lines of stressLarge, bony projections occur where heavy, active muscles attachFigure 6.13Load here (body weight)Head offemurCompressionherePoint ofno stressTensionhereClassification of Bone Fractures Bone fractures may be classified by four “either/or” classifications:Position of bone ends after fracture:Nondisplaced—ends retain normal positionDisplaced—ends out of normal alignmentCompleteness of the breakComplete—broken all the way throughIncomplete—not broken all the way throughClassification of Bone FracturesOrientation of the break to the long axis of the bone:Linear—parallel to long axis of the boneTransverse—perpendicular to long axis of the boneWhether or not the bone ends penetrate the skin:Compound (open)—bone ends penetrate the skinSimple (closed)—bone ends do not penetrate the skinCommon Types of FracturesAll fractures can be described in terms ofLocationExternal appearanceNature of the breakTable 6.2Table 6.2Table 6.2Stages in the Healing of a Bone FractureHematoma formsTorn blood vessels hemorrhageClot (hematoma) forms Site becomes swollen, painful, and inflamedFigure 6.15, step 1A hematoma forms.1HematomaStages in the Healing of a Bone FractureFibrocartilaginous callus formsPhagocytic cells clear debrisOsteoblasts begin forming spongy bone within 1 weekFibroblasts secrete collagen fibers to connect bone endsMass of repair tissue now called fibrocartilaginous callusFigure 6.15, step 2 Fibrocartilaginouscallus forms.2ExternalcallusNewbloodvesselsSpongybonetrabeculaInternalcallus(fibroustissue andcartilage)Stages in the Healing of a Bone FractureBony callus formationNew trabeculae form a bony (hard) callusBony callus formation continues until firm union is formed in ~2 monthsFigure 6.15, step 3Bony callus forms.3Bonycallus ofspongyboneStages in the Healing of a Bone FractureBone remodelingIn response to mechanical stressors over several monthsFinal structure resembles originalFigure 6.15, step 4 Bone remodelingoccurs.4HealedfractureFigure 6.15HematomaExternalcallusBonycallus ofspongyboneHealedfractureNewbloodvesselsSpongybonetrabeculaInternalcallus(fibroustissue andcartilage)A hematoma forms. Fibrocartilaginouscallus forms.Bony callus forms. Boneremodelingoccurs.1234Homeostatic ImbalancesOsteomalacia and ricketsCalcium salts not depositedRickets (childhood disease) causes bowed legs and other bone deformitiesCause: vitamin D deficiency or insufficient dietary calciumHomeostatic ImbalancesOsteoporosisLoss of bone mass—bone resorption outpaces depositSpongy bone of spine and neck of femur become most susceptible to fractureRisk factorsLack of estrogen, calcium or vitamin D; petite body form; immobility; low levels of TSH; diabetes mellitusFigure 6.16Osteoporosis: Treatment and PreventionCalcium, vitamin D, and fluoride supplements Weight-bearing exercise throughout lifeHormone (estrogen) replacement therapy (HRT) slows bone loss Some drugs (Fosamax, SERMs, statins) increase bone mineral densityPaget’s DiseaseExcessive and haphazard bone formation and breakdown, usually in spine, pelvis, femur, or skullPagetic bone has very high ratio of spongy to compact bone and reduced mineralizationUnknown cause (possibly viral)Treatment includes calcitonin and biphosphonatesDevelopmental Aspects of BonesEmbryonic skeleton ossifies predictably so fetal age easily determined from X rays or sonogramsAt birth, most long bones are well ossified (except epiphyses)Figure 6.17Parietal boneRadiusUlnaHumerusFemurOccipital boneClavicleScapulaRibsVertebraIliumTibiaFrontal boneof skull MandibleDevelopmental Aspects of BonesNearly all bones completely ossified by age 25Bone mass decreases with age beginning in 4th decadeRate of loss determined by genetics and environmental factors In old age, bone resorption predominates