BONE STRUCTURE AND ITS CLINICAL IMPORTANCE

Dr GIRIDHAR BOYAPATI P.G

What is Bone? – Mineralized connective tissue

- constitute part of the endoskeleton of vertebrates

Classification

REGION- Axial, Appendicular

SHAPE - Long bones, short bones, irregular, pneumatic, sesamoid, accessory

STRUCTURE Macroscopic – Compact

Spongy

Microscopic – Lamellar (Secondary Bone) Woven/fibrous(Primary Bone)

DEVELOPMENT – Membranous Cartilaginous

Membrano-cartilaginous

ENDOCHONDRAL OSSIFICATION

MESENCHYMAL CELLS

CHONDROBLASTS

CHONDROCYTES

CARTILAGE MODEL OF FUTURE BONE

OSTEOBLASTS

Endochondral Ossification

Endochondral Ossification

Endochondral Ossification Defects – AD Inheritance

• Achondroplasia

• Thanatophoric Dysplasia

• Hypochondroplasia

Mutation in FGFR 3 gene

Intramembranous Ossification

EXAMPLES OF INTRAMEMBRANOUS OSSIFICATION

1. EMBRYONIC FLAT BONES : SKULL, PELVIS, MAXILLA, MANDIBLE, CLAVICLE

2. DISTRACTION OSTEOGENESIS

3. FRACTURE HEALING WITH RIGID FIXATION

4.BLASTEM BONE

PERIOSTEAL OSSIFICATION

OSTEOGENIC CELLS FROM PERIOSTEUM

LAY PARLLEL LAYERS OF COMPACT BONE

Bone cells

Osteo progenitors(Pleuripotent stem cells)

Osteoblasts ("bone makers")

Osteocytes ("bone cells")

Osteoclasts (“bone breakers”) remodeling

MATRIXGround substance

ProteoglycansGlycoproteinsMineralsWater

Fibers

Cells of Bone (Primary/Temporary)

Osteoprogenitor

Osteoclast

Osteoblast

Osteocyte

Osteoid

PERIOSTEUM

MEMBRANE COVERING OUTER SURFACE OF BONE

LAYERS: 1. FIBROUS LAYER 2. CAMBIUM LAYER

OSTEOGENIC CELLS

OSTEOBLAST

OSTEOCYTE

OSTEOCLAST

Osteoclast

CANALICULI

Bone cells -Function• Osteoblasts – Matrix synthesis – Osteoid,

Calcification

PTH receptors

• Osteocyte – Maintanace of Matrix by intercellular sickling systems

• Osteoclast – Digestion of collagen, dissolving hydroxyapatite

* Calcitonin receptors

Bone cells- Medical applicationRate of bone apposition – Bone growth

Osteomalacia – Impaired mineralization

Osteitis fibrosa cystica – osteoclast activityOsteopetrosis – “Marble bones” – Bone resorption

defect due to osteoclastic activityOsteitis deformans (Paget’s disease) –Uncontrolled

osteoclast activity followed by osteoblastic activity (incomplete)- Stops at osteoid level

BIOCHEMISTRY

1.INORGANIC 65 -70%2.ORGANIC 30-35%

ORGANIC: a. collagen 90-95% b. pps 4-5% c.Lipids 0.1% INORGANIC 90% Calcium and phosphate

BONE COLLAGEN

1.AXIAL PERIODICITY OF 640 TO 700A

2.PROTIEN COMPOSITION WITH ONE THIRD GLYCINE

3.LARGE NO. OF ALANINE RESIDUES

4.CYSTEINE IS COMPLETELY ABSENT

Matrix

• Fibers – Collagen Type I- Gene mutation in alfa 1or 2 OSTEOGENESIS IMPERFACTA

• Ground substance

Proteoglycans – Chondroitin Sulphate, Keratan Sulphate

Glycoproteins – Osteocalcin , Alkaline phosphatase

Structural regions of long bone

Gross structure of typical long bone Shaft – Thick compact bone+ medullary cavity Ends- Cancellous bone + thin compact layer Articular cartilage – No periosteum, avascular Periosteum – Fibrous + cellular

Shape, nutrition, attachment

fracture repair, sensitive Endosteum – Cellular -Repair

and remodelling Nutrient foramen – mid shaft Bone marrow – Red, Yellow

Parts of a growing bone

Epiphysis

(Secondary) Epiphyseal

plate Metaphysis Diaphysis

(Primary)

TYPES OF EPIPHYSIS

PRESSURE

region of the long bone that forms the joint is called Pressure Epiphysis

ARTICULAR....WT TRANSMISSON

EX: HEAD OF FEMUR AND HUMERUS

TRACTIONNon-articularMuscle pullOssifies later than Pressure

.EX HUMERUS G.T AND L.T FEMUR G.T AND LT

ATAVISTICCOROCOID PROCESS OF SCAPULAOS TRIGONUM

ABERRANTHEAD OF 1ST METACARPEL

Unusual

Epiphyseal plate

Growth Plate

ZONE 1INJURY CAUSES CESSATION OF GROWTH

ZONE 2BONE LENGTH IS ADDED

ZONE 3WEAKEST PORTION OF GROWTH PLATE

Metaphysis

Epiphyseal end of diaphysis

Active growth Before fusion

end arteries, hair pin bends

OSTEOMYELITIS

Blood supply of bones

Long Bone Nutrient artery Metaphyseal arteries Epiphyseal arteries Periosteal arteries

Short Bone - Nutrient artery; Periosteal arteries

Vertebra- Body, Processes

Rib - Nutrient artery; Periosteal arteries

Nutrient artery Mid shaft Tortuiosity 2/3rd inner compact bone Hair pin loops Direction – away from

growing end

.

“To the elbow I go. From the knee I flee.”

Nutrient Artery

1.Enters into the diaphysis of long bones through an oblique canal

2.direction of canal is determined by relative amount of growth that has occurred at proximal and distal ends of the bone;

3.does not branch within the cortex, divides after reaching the medullary cavity,

4. direction of blood flow is centrifugal;

Disruption of Nutrient Artery causes

1. In growing bone can result in necrosis of large portion of marrow & of inner two thirds of cortex

2. This cortical death does not occur in adult bone because combined epiphyseal-metaphyseal collateral circulation is developed enough to maintain these areas;

3.loss of circulation in terminal vessels of nutrient artery of growing bone will interfere with enchondral ossification;

Epiphyseal arteries

In femoral and radial heads, which are almost entirely covered by cartilage vessels enter in region between articular cartilage & growth-plate cartilage

In other regions, the epiphysis has openings that permit passage of large number of vessels into and out of the ossification centers

Obliteration of epiphyseal blood supplycauses

1.necrosis of epiphysis

2. longitudinal growth ceases

3. permanent closure of epiphyseal plate

METAPHYSIAL ARTERIES

BRANCHES OF SYSTEMIC VESSELS

Epiphyseal vessels are responsible for permitting longitudinal growth to occur, whereas metaphyseal vessels nourish

osteoprogenitor cells, which lay down bone on cartilage matrix;

PERIOSTEAL ARTERIES

Periosteal vessels send small branches thru minute channels in cortex to supply about outer 1/3 of cortex

Extensive network of vessels covers entire length of the bone shaft

Anastomoses with adjacent skeletal muscles so in cases in which the nutrient artery of muscle has been damaged, then periosteal vessels may temporarily serve as the primary blood supply;

BLOOD SUPPLY OF GROWTH PLATE

growth plate itself is avascular & receives nutrition from 2 sources

1.epiphyseal vessels that supply germinal, proliferating, and upper hypertrophic cell layers by diffusion

2 .metaphyseal vessels that supply zone of provisional calcification

In a young child, epiphyseal vessels are separated from metaphyseal vessels, but

following growth arrest of the cartilage plate, there is

an extensive anastomoses between epiphyseal vessels, metaphyseal vessels, &

terminal branches of Nutrient Artery;

VENOUS DRAINAGE

TRANSVERSE VENOUS CHANNELS

CENTRAL VENOUS SINUS

NUTRIENT VEIN

-ONLY 5-10% OF VENOUS DRINAGE IS THROUGH NUTRIENT VEIN

-REMAINING IS THROUGH PERIOSTEAL VENOUS DRINAGE

Circulatory disturbances

PHYSIS AND EPIPHYSIS1.Legg–Calve–Perthes Disease: Circulatory disturbance to the capital

femoral epiphysis 2.Physeal TraumaMETAPHYSIS1.Haematogenous Osteomyelitis2.Metastasis.DIAPHYSIS1.Intramedullary Reaming2.Fracture HealingPERIOSTEAL BLOOD SUPPLY1.Paralytic conditions

Spongy bone

1. loose network of bone trabecule

2. interconnected

3. arranged along lines of maximum stress

Spongy Bone

Superimposed lamllaeNo Haversian systemLamellated trabeculae Red marrow

Spongy Bone- No HS

Osteon (Haversian system) Central canal (Haversian

or osteonal canal) Transverse (Volkmann)

canals Lacuna Canaliculi ("tiny canals") Lamellae

Concentric,Intersititial,

Circumferential

Compact bone

COMPACT BONE

Sharpey’s fibers

Connective tissue matrix

Bundles of collagen fibers Connect Perisoteum to Bone

Fibrous layer of Periosteum to outer circumferential and interstitial lamellae

Growing Bone

BONE GROWTH1. Appositional

2. Endochondral

Factors affecting growth of a bone

Nutritional Vit. A - Co-ordination of osteoblastic and

osteoclastic activity

Vit.C – Synthesis of organic matrix

Vit.D – Absorption of Ca, P

Rickets, Osteomalacia (Calcification deficiency)

Calcium – Decalcification of bone

Factors affecting growth of a bone

Hormonal – • Pituitary - GH- Dwarfism; Gigantism,

Acromegaly• Thyroid - Calcitonin

Parathyroid – PTH Decalcification

Sex Hormones - Androgens, estrogens - Stimulators Mechanical factors

Tensile forces – Bone formation

Compressive forces – Bone resorption

Ossification Centre

Rules of Ossification Primary centers - before birth

except carpal and tarsal (except calcaneus, talus, cuboid)

Secondary centers - after birth

except lower end of femur, upper end of tibia, humerus

Center which appears first unites last

except lower end of FIBULA

Rules of Ossification Center which appears later unites first

except upper end of fibula Direction of nutrient artery - away from

growing end

except fibula Growing end is one where center

appears first and unites last

except fibula

Fracture Healing1. Hematoma

formation Macrophages

Osteoclasts2. Fibrocartilaginous

callus formation Periosteum Endosteum 3. Bony callus

formation Ossification (EC & IM)4. Remodeling Sec.bone formation

Bone remodeling cycle