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Calcium homeostasis of blood: 9–11 mg/100 ml. BALANCE. BALANCE. Stimulus Falling blood Ca 2+ levels. Thyroid gland. Osteoclasts degrade bone matrix and release Ca 2+ into blood. Parathyroid glands. Parathyroid glands release parathyroid hormone (PTH). PTH. Figure 6.12. - PowerPoint PPT Presentation



Figure 6.12

Osteoclastsdegrade bonematrix and release Ca2+into blood.ParathyroidglandsThyroidglandParathyroidglands releaseparathyroidhormone (PTH).StimulusFalling bloodCa2+ levelsPTHCalcium homeostasis of blood: 911 mg/100 mlBALANCEBALANCECopyright 2010 Pearson Education, Inc.Hormonal Control of Blood Ca2+May be affected to a lesser extent by calcitonin Blood Ca2+ levelsParafollicular cells of thyroid release calcitoninOsteoblasts deposit calcium salts Blood Ca2+ levelsLeptin has also been shown to influence bone density by inhibiting osteoblastsCopyright 2010 Pearson Education, Inc.Response to Mechanical StressWolffs law: A bone grows or remodels in response to forces or demands placed upon itObservations supporting Wolffs 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 attachCopyright 2010 Pearson Education, Inc.Figure 6.13

Load here (body weight)Head offemurCompressionherePoint ofno stressTensionhereCopyright 2010 Pearson Education, Inc.Classification of Bone Fractures Bone fractures may be classified by four either/or classifications:Position of bone ends after fracture:Nondisplacedends retain normal positionDisplacedends out of normal alignmentCompleteness of the breakCompletebroken all the way throughIncompletenot broken all the way throughCopyright 2010 Pearson Education, Inc.Classification of Bone FracturesOrientation of the break to the long axis of the bone:Linearparallel to long axis of the boneTransverseperpendicular 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 skinCopyright 2010 Pearson Education, Inc.Common Types of FracturesAll fractures can be described in terms ofLocationExternal appearanceNature of the breakCopyright 2010 Pearson Education, Inc.Table 6.2

Copyright 2010 Pearson Education, Inc.Table 6.2

Copyright 2010 Pearson Education, Inc.Table 6.2

Copyright 2010 Pearson Education, Inc.Stages in the Healing of a Bone FractureHematoma formsTorn blood vessels hemorrhageClot (hematoma) forms Site becomes swollen, painful, and inflamedCopyright 2010 Pearson Education, Inc.Figure 6.15, step 1

A hematoma forms.1HematomaCopyright 2010 Pearson Education, Inc.Stages 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 callusCopyright 2010 Pearson Education, Inc.Figure 6.15, step 2

Fibrocartilaginouscallus forms.2ExternalcallusNewbloodvesselsSpongybonetrabeculaInternalcallus(fibroustissue andcartilage)Copyright 2010 Pearson Education, Inc.14Stages 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 monthsCopyright 2010 Pearson Education, Inc.Figure 6.15, step 3

Bony callus forms.3Bonycallus ofspongyboneCopyright 2010 Pearson Education, Inc.Stages in the Healing of a Bone FractureBone remodelingIn response to mechanical stressors over several monthsFinal structure resembles originalCopyright 2010 Pearson Education, Inc.Figure 6.15, step 4

Bone remodelingoccurs.4HealedfractureCopyright 2010 Pearson Education, Inc.Figure 6.15

HematomaExternalcallusBonycallus ofspongyboneHealedfractureNewbloodvesselsSpongybonetrabeculaInternalcallus(fibroustissue andcartilage)A hematoma forms. Fibrocartilaginouscallus forms.Bony callus forms. Boneremodelingoccurs.1234Copyright 2010 Pearson Education, Inc.Homeostatic ImbalancesOsteomalacia and ricketsCalcium salts not depositedRickets (childhood disease) causes bowed legs and other bone deformitiesCause: vitamin D deficiency or insufficient dietary calciumCopyright 2010 Pearson Education, Inc.Homeostatic ImbalancesOsteoporosisLoss of bone massbone 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 mellitusCopyright 2010 Pearson Education, Inc.Figure 6.16

Copyright 2010 Pearson Education, Inc.Osteoporosis: 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 densityCopyright 2010 Pearson Education, Inc.Pagets 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 biphosphonatesCopyright 2010 Pearson Education, Inc.Developmental 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)Copyright 2010 Pearson Education, Inc.Figure 6.17

Parietal boneRadiusUlnaHumerusFemurOccipital boneClavicleScapulaRibsVertebraIliumTibiaFrontal boneof skull MandibleCopyright 2010 Pearson Education, Inc.Developmental 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 predominatesCopyright 2010 Pearson Education, Inc.