Bone phisiology
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Bone phisiology

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I have described most of the things related to bone physiology so you can take the important things to stduy what you think from this seminar.

I have described most of the things related to bone physiology so you can take the important things to stduy what you think from this seminar.

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  • -Bone is highly vascular, living, constantly changing, mineralized connective tissue.-Sesamoid bone are the bones embedded within tendon. Found in hand, knee and foot. Eg patella.-They act to protect the tendon and increase its mechanical effect.
  • -Supports soft tissues and provide attachment for tendons of most skeletal muscles.-Bone protects many internal organs from injury eg. Skull protect brain.-Red bone marrow (medulla ossiumrubra) consist mainly of hematopoietic tissue. Found mainly in flat bones.-Yellow bone marrow (medulla ossiumflava) : consist mainly of adipose cells which stores triglycerides, which body use as a last reservior in cases of extreme starvation.
  • Flat bones- skull, sternum, pelvis and ribs.Long bones- bones of limbs.Irregular bones- face bone and vertebral column.Short bones- bones of hands and feets such as phalanges, metacarpals and metatarsals.Accessory or supernumerary bone- extra bone that develop in additional ossification centers failed to fuse with main parts during development. These bones may be mistaken for bone chips or fractures.
  • epiphysis – its is the region between the growth or growth plate scar and the expanded end of bone, covered by articular cartilage. It is present at both the ends of bone except clavical, ribs, phalanges proximal end, proximal first and distal second through fifth meta carpals and pfads through fifth metatarsals.Carpal, tarsal bones and patella are also called epiphysioid bones and are developmentally equivalent to epiphysis of long bones.Metaphysis – this region is a comman site for many primary bone tumors and similar lesions.Diaphysis – located in the region between metaphyses.Physis – seperates epiphysis from metaphysis. It is zone of endochodral ossification.
  • -Endosteum is made up of loose irregular connective tissue, with osteoblast and osteoclast. It is highly vascular condensation of areolar tissue lining various medullary spaces.Long b ones include- femora, tibiae and fibulae of the legs; humeri, radii and ulnae of the arms; metacarpals and metatarsals of hands and feet;phalanges of fingers and toes and the clavicals or the collar bone, mandible.
  • Forms cortex or outer shell of most bones.Present between osteogenic layer of periosteum and spongy bone.Chifly consist of calcium phosphate and type 1 collagen.. These are arranged in concentric circles around central haversian canal.
  • It is primary anatomical and functional unit of cortical bone.Osteon- consist of concentric layers of lamellae of compact bone tissue that surrounds a central canal, Haversian canal, which contains blood and nerve supply to bone.The boundry of the osteon is CEMENT LINE.Osteons are connected to each other and the periosteum bye oblique channels called volkman’s canals or perforating canals.
  • Also known as cancellous boas compared to compact bone it has higher surface area, is less dense, softer, weaker and less stiff.Found in ends of long bones, proximal to joints and within the interior of vertebrae.
  • - The alveolar process contains a region of compact bone adjacent to the periodontal ligament called lamina dura- It is stated that in the posterior maxilla; the trabeculae are typically thin, and numerous, forming a fine, granular, dense pattern, and the marrow spaces are consequently slightly larger than the anterior region of the maxilla and relatively numerous. In the posterior mandible, the periradiculartrabeculae are somewhat thicker than in the maxilla resulting in a coarser pattern and they are relatively larger than the trabeculae in the anterior region of the mandible. The trabecular plates in the mandible are also fewer than in the maxilla and marrow spaces are correspondingly larger
  • It is also an pathologic tissue in adults, except in few places such as near the suture of the flat bones of skull, tooth sockets.
  • In diagram - One small and 1 large plasma cell in top left frame. 2 osteoblasts in top right frame, 1 osteoblast in lower frame.cuboidal and columnar in shape with a central nucleus.found on the bone surface. osteoblasts come from the poorly differentiated mesenchymal cell of the internal osteogenic layer of periosteum and the bone marrowThey have receptors for hormones such as vitamin D, estrogen, and parathyroid hormone.  secrete factors that activate osteoclasts (RANK-ligand) secrete PHEX, a protein that helps to regulate the amount of phosphate excreted by the kidney. Procollagen molecules are produced bythe ribosomes and extruded into extracellular space , proteolysis and polymerization within the extracellular space results in formation of collagen fibrils. - Combination of thes extracellular and intracellular events leads to production of osteoid seam.
  • osteocyte, mature bone cells, a star shaped cellOsteocytes have an average half life of 25 years, they do not divide, and they are derived from osteoprogenitors, some of which differentiate into active osteoblastsCells contain a nucleus and a thin ring piece of cytoplasm. space that an osteocyte occupies is called a lacuna Osteocytes are networked to each other via long cytoplasmic extensions that occupy tiny canals called canaliculi, which are used for exchange of nutrients and waste through gap junctions-These have also been show to act as mechanosensoryreceptars regulating the bones response to stress and mechanical load.
  • Precursors (blood monocytes) circulate in the blood and bone marrow. formed from fusion of the precursors. happens when RANK receptors on the osteoclast precursors are activated by the RANK-ligand which was secreted by osteoblasts. Osteoprotegerin (OPG) is a factor in the marrow which also binds RANK-ligand, so it can help to regulate the osteoclast activation. After they finish resorbing bone, they undergo apoptosis (programmed cell death, sometimes called 'cell suicide'). This process is regulated by proteins from other cells.
  • Nerve supply: Hilton’s law: according to this law nerve supplying a muscle will aslo supply the underlying bone.Most of the nerves coming to bone are sympathetic(activate fight or flight response) and vasomotor(causing or regulating dilation or constriction of blood vessels) in function.Some nerves are sensory and are distributed to the articular ends and the periosteum
  • At periphery of cartilage mesenchymal cells continue to proliferate and differentiate. Called as appositiona growth.In interstitial growth cell proliferation and synthesis of new matrix between chondrocytes occur.
  • Begin to form at epiphyseal ends.By similar process , as in development of primary ossification center , trabecular bone and marrow space are formed at these ends..
  • Zone of resting cartilage- cells separated by abundant extracellular matrix and have less tendancy to proliferate.Zone of proliferating cartilage- chondroblast divide actively forms groups and actively synthesize the matrixUpperZone of hypertrophic cartilage- increased vacuolation of cells. Matrix synthesis increased 3 fold compared to proliferative zone.
  • bone in a healthy person or animal will adapt to the loads under which it is placed.If loading on a particular bone increases, the bone will remodel itself over time to become stronger to resist that sort of loading. The internal architecture of the trabeculae undergoes adaptive changes, followed by secondary changes to the external cortical portion of the bone,perhaps becoming thicker as a result. The inverse is true as well: if the loading on a bone decreases, the bone will become weaker due to turnover, it is less metabolically costly to maintain and there is no stimulus for continued remodeling that is required to maintain bone mass.
  • It is refinement of wolfs law.Mechanostat is model describing bone growth and bone loss.
  • Bennighof studied the natural line of stress in skull by piercing small holes into fresh skulls.When skull were dried he observed holes assumed a linear form in the direction of bony trabeculae these were called benninghoff’s line or trajectories.It indicates direction of functional stresses
  • Canine lines run superiorly by the sides of piriform aperture and crest of nasal bone to frontal boneZygomatic lines runs inferiorly along the orbit,superiorly along the lateral wall of orbit,runs along the zygomatic arch.In mandible it radiates from beneath the teeth in the alveolar process & join common stress pillar that terminates in condyle.Lower border and mylohyoid ridges are other prominent buttresses of mandible.
  • Insulin-like growth factors (IGFs): These growth factors are produced by osteoblastic cells in response to several bone active hormones, such as parathyroid hormone and estrogens, or BMPs. Growth factorsBone morphogenetic proteins (BMPs): BMPs are produced in the bone or bone marrow. They bind to BMP receptors that are on mesenchymal stem cells within the bone marrow. This causes the cells to produce Cbfa 1, which is a factor that activates the DNA so proteins can be made -- a process known as gene transcription. When Cbfa 1 activates the genes, the cells differentiate into mature osteoblasts. Without Cbfa 1, the cells would turn into fat cells instead!IGFs accumulate in the bone matrix and are released during the process of bone remodeling by osteoclastsCytokinesInterleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor (TNF) family of cytokines: These factors are produced by osteoblastic cells in response to systemic hormones or other cytokines. IL-6 can cause: * Bone marrow stem cells to differentiate into pre-osteoclasts * Changes in proliferation and differentiation of osteoblasts * Inhibition of apoptosis of osteoblastsRANKL (RANK-ligand) is a cytokine that stays on the surface of osteoblast-related cells.
  • Parfit states that a fully developed BMU consists of a team of osteoclasts forming the cutting cone or hemicone, a team of osteoblast forming the closing cone, some boold vessels and associated connective tissue
  • The cutting head is stimulated by inflammatory cytokines produced by osteocytes in damagedbone (left). Preosteoclasts have RANK receptors that are bound and activated by RANKL, probably produced ormediated by T cells (lymphocytes) near the resorption front. Growth factors from resorbed bone (bottom)stimulate production of preosteoblasts, which then produce OPG to block the RANK receptors on osteoclasts;the latter then withdraw from the scalloped surface and degenerate. Relatively flat mononuclear cells (bottomcenter) form cementing substance to form a resorption arrest line. Osteoblasts (bottom right) produce newlamellar bone to fill the resorption cavity.
  • Regional accelerIt is an important reaction of bone Any regional noxious stimulus can evoke RAPMost of the active vital processes are accelerated like perfusion,growth of bone cartilage ,BMU turnover of woven & lamellar bone ,turnover of connective tissueWhen RAP fails to develop ,healing is delayed & infection progressesDuration of RAP is in the range of months to years

Bone phisiology Bone phisiology Presentation Transcript

  • PRESENTED BY – DR. PARAG S. DESHMUKH
  • CONTENTS • Introduction • Function • Classification of bone • Bone composition • Bone morphology • Bone ossification • • • Bone physiology Conclusion Refrence
  • INTRDUCTION  The Adult human skeleton has a total of 206 bones, excluding the sesamoid bone. AUDITORY 6 206 BONES APPENDICULAR SKELETON 126  AXIAL 74 Each bone constantly undergoes modeling during life to help it adapt to changing biomechanical forces as well as remodeling to remove old, microdamaged bone and replaced it with new, mechanically stronger bone to help preserve bone strength.
  • Functions of Bone Supports & protects soft tissues Store minerals (Ca & P) – mineral homeostasis Blood cell production (hemopoiesis) in red bone marrow. Energy storage -- yellow bone marrow Buffering action – buffers blood by absorbing or releasing alkaline salts . Detoxification – Bones can store heavy metals and foreign elements, removing them from blood and reducing there effects on other organs.
  • Bones are Classified based on shape and structure
  • Based on location AXIAL SKELETON APPENDICULAR SKELETON ACRAL SKELETON • Bones of skull, vertebral column, sternum and ribs • Bones of pectoral griddle, pelvis gridle and limbs • It‟s a part of appendicular skeleton and includes bones of hands and feets.
  • Gross structure of long bones Articular cartilage = covers joint surfaces, reduces friction and absorbs shock Epiphysis : End of long boes. Metaphysis = area between epiphyses & diaphysis includes epiphyseal plate in growing bones Diaphysis = Shaft of long bones. Medullary cavity = marrow cavity Physis = epiphyseal growth plate
  • • Endosteum = lining of marrow cavity • Periosteum = tough membrane covering bone  Fibrous layer: Fibrous and madeup of dense irregular CT  Osteogenic layer: contains many osteoblasts & blood vessels that nourishes bone
  • TYPES OF BONE TISSUE  Based on texture of cross sections  Compact bone(dense bone or cortical bone)  Spongy bone(trabecular bone, cancellous bone)
  • Cortical bone Represents 80% of skeletal mass • Has slower turnover rate and high resistance to bending and torsion Contains series of adjacent and overlapping bulls eye formations known as, haversian system or osteon. Between each osteons are interstitial lamellae(concentric layer of mineralized bone) Haversian canals communicate with medullary cavity through spaces in spongy bone and with the surface of bone by oblique or transverse channels called as VOLKMAN‟S CANAL.
  • Compact Bone
  • Haversian system / Osteon
  • SPONGY BONE Located along the epiphyses of long bones Site of Erythrocyte (RBC) formation Collagen fibers are not arranged in concentric rings. But the lamellae form rods called TRABACULAE. No Osteons or Haverian Systems are present. Found in short, flat, irregular bones & epiphyses of long bones. Supports and protect red bone marrow It is less dense, more elastic and has a higher turnover rate Trabeculae follows lines of stresses and can realign if the lines of stress changes.
  • Trabeculae of Spongy Bone
  • BASED ON MATRIX ARRANGEMENT  LAMELLAR BONE (SECONDARY BONE TISSUE) • Matur bone with collagen fibers that are arranged in lamellae • In spongy bone lamellae are arranged parellel to each other. • In compact bone lamellae are concentrically organized around vascular canal.
  • WOVEN BONE (PRIMARY BONE TISSUE) • It is immature bone, in which collagen fibers are arranged in regular random arrays and contain smaller amounts of mineral substance and higher proportion of osteocytes than lamellar bone • It is temporary bone. • Eventually gets converted to lamellar bone.
  • BASED ON MATURITY  IMMATURE BONE (Primary bone tissue)  It is woven bone.  Mature bone(Secondary bone tissue)  It is charectiristically lamellar bone  Almost all bone in adults are lamellar bone
  • Histology of Bone Tissue Bone: CT of widely-spaced cells separated by matrix Matrix = 25% water, 25% collagen fibers, & 50% crystallized mineral salts 4 types of cells in bone : osteogenic cells osteoblasts osteocytes osteoclasts
  • Matrix Contains inorganic mineral salts & protein - mostly hydroxyapatite( calcium phosphate ) - some calcium carbonate, K, Mg - collagen fibers Mineral salts deposited in a framework of collagen fibers - calcification(=mineralization gives bone hardness ) - collagen fibers give bone great tensile strength –
  • BONE  Organic Framework Osteoblasts, osteocytes, osteoclasts  Collagen  Other organic molecules   Inorganic Salts calcium and phosphorus keep bone rigid  Bone stores minerals and ions for body functions 
  • Non – collagenous organic components Osteonectin – Phosphorylated glycoprotein secreted by osteoblasts, binds to collagen & hydroxyappatite, play a role in hydroxy appatite crystallization. Osteocalcin – Glycoprotein synthesized by osteoblasts, binds hydroxyappatite & Ca, used as a marker of new bone formation. Bone proteoglycans biglycan & decorin may bind transforming growth factor–β (TGF-β). Bone sialoproteins, osteopontin & thrombospondin mediate osteoclast adhesion to bone surfaces via binding to osteoclast integrins.
  • Bone matrix also contains many growth factors, proteases & protease inhibitors which are secreted by osteoblasts, often in a latent form. Transforming growth factor-β (TGF-β), secreted by osteoclasts as well as osteoblasts, is activated in the acid conditions of the ruffled border zone of the osteoclast, & may be a coupling factor for new bone formation at resorption site.
  • Osteoprogenitor or Osteogenic cells  Appearance  pale staining,  small, spindle shaped  Location    present on all nonresorbing surfaces in lacunae within bone. Extends protoplasmic processes into small canaliculiin intercellular matrix. periosteum and endosteum Function give rise to osteoblasts in vascularized regions chondroblasts in avascular regions
  • Osteoblasts  Appearance      large, nondividing cells, eccentric nucleus, basophilic cytoplasm, cytoplasmic processes Function   synthesize and secrete organic constituents of bone matrix (osteoid) aid in calcification
  • Osteocyte  Appearance    smaller and less basophilic than osteoblast, have interconnecting processes Function   keeps bone matrix in good repair release calcium ions from bone matrix when calcium demands increase
  • Osteoclasts  Appearance     multinucleated, non-dividing cells, acidophilic. Have a ruffled border and a clear zone on front of resorption side.  Origin   From blood monocytes/ macrophages Function    move around on bone surfaces, resorbs bone matrix Focal decalcification and extracellular digestion by acid hydrolases and uptake of digested material
  • Blood & Nerve Supply of Bone
  • BONE FORMATION (OSSIFICATION) • . It is a process of formation of bone and it includes proliferation of collagen and ground substance with subsequent deposition of calcium salts.  Two types  Intramembranous  Endochondral ossification ossification
  • INTRAMEMBRANOUS OSSIFICATION  It is the direct laying down of bone into the primitive connective tissue(Mesenchym).  It results in formation of cranial bones of the skull and the clavicles  All bones formed this way are flat bones  It is also an important process during natural healing of bone fractures
  • Stages of Intramembranous Ossification
  • Stages of Intramembranous Ossification
  • Stages of Intramembranous Ossification
  • Stages of Intramembranous Ossification
  • Endochondral Ossification  Results in the formation of all of the rest of the bones  Begins in the second month of development  Uses hyaline cartilage “bones” as models for bone construction  Requires breakdown of hyaline cartilage prior to ossification
  • 1. Development of Cartilage Model  Mesenchyme forms cartilage model of bone during development  There is an aggregation of mesechymal cells  Mesenchymal cells differentiate into chodroblasts.  These chondroblast secret hyaline cartilage matrix
  • 2. Growth of Cartilage Model Cartilage grows by both :  interstitial (mostly in length)  Appositional(mostly in width)  Sometimes during growth of cartilage model some of Inner perichondral cells gives rise to osteoblast instead of chondroblast (as a result fomer perichondrium is now called the periosteum).  Newly formed osteoblast secret osteoid forming bone collar around cartilage model.
  • 3. Development of Primary Ossification Center Chondrocytes differentiate and become hypertrophic. Then it deposits mineralized matrix. Cartilage calcification is initiated by matrix vesicles Calcified matrix is partially resorbed by osteoclast. After resorption osteoblast differentiate into this area forming woven bone layer. Blood vessels enter in this area. And penetrate bone to allow seeding of bone marrow.
  • 4. Development of the Medullary ( Marrow) Cavity Osteoblasts deposit matrix over calcified cartilage form trabeculae of spongy bone Osteoclasts form medullary cavity
  • 5) Development of Secondary ossification centre
  • Formation of Articular Cartilage & Epiphyseal Plate 6. • Cartilage on epiphyses remains as articular cartilage • Epiphyseal (growth) plate also remains as cartilage
  • - source of interstitial growth
  • 4 Zones of Epiphyseal Plate: Zone of resting cartilage Zone of proliferating cartilage Zone of hypertrophic cartilage Zone of calcified cartilage
  • Zone of resting cartilage anchors growth plate to bone Zone of proliferating cartilage rapid cell division (stacked coins) Zone of hypertrophic cartilage cells enlarge & remain in columns Zone of calcified cartilage thin zone of mostly dead cells osteoclasts remove matrix osteoblasts & capillaries build bone over calcified cartilage
  • Factors Affecting Bone Growth Nutrition: need adequate levels of minerals & vitamins  - Ca & P for bone growth  - vitamin C for collagen synthesis  - vitamins K & B12 for protein synthesis Need adequate levels of specific hormones  - insulinlike growth factor ( IGF) needed during childhood  - promotes cell division at epiphyseal plate  - also need hGH, thyroid (T3 & T4) , & insulin  - sex hormones needed at puberty (estrogen & testosterone):  - stimulate growth & male/female skeletal modifications
  • BONE PHYSIOLOGY  Eugene Roberts referred orthodontists as craniofacial bone specialist and hence torough knowledge about bone physiology will help us to treat patients more effectively and efficiently.
  • BONE REGULATORS ENDOCRINE REGULATORS: PTH harmone Calcitonin Vitamin D Vitamin A Estrogens Androgens
  • Growth factors Paracrine regulators Autocrine regulators Neurotransmitters • Bone morphogenetic protein(BMP) • Insulin-like growth factors • Transforming –growth factors • Platelet derived growth factor • Fibroblast growth factor • RANKL (produced locally) • OPG Produced intracellularly.
  • WOLF‟S LAW Wolff's law is a theory developed by the German anatomist and surgeon Julius Wolff (1836–1902) in the 19th century that states that Bone reacts to mechanical functional stress through an adaptive process resulting in a change of its external and internal architecture to better withstand this stress. If loading on a particular bone increases, the bone will remodel itself over a period of time to become stronger to withstand greatest strength with least amount of material
  • Mechanotransduction The remodeling of bone in response to loading is achieved via mechanotransduction, a process through which forces or other mechanical signals are converted to biochemical signals in cellular signaling. The specific effects on bone structure depends on the duration, magnitude and rate of loading, and it has been found that only cyclic loading can induce bone formation When loaded, fluid flows away from areas of high compressive loading in the bone matrix
  • Mechanotransduction Osteocytes are the most abundant cells in bone and are also the most sensitive to such fluid flow caused by mechanical loading Upon sensing a load, osteocytes regulate bone remodeling by signaling to other cells with signaling molecules or direct contact Additionally, osteoprogenitor cells, which may differentiate into osteoblasts or osteoclasts, are also mechanosensors and may differentiate one way or another depending on the loading condition.[
  • Example:  Weightlifters often display increases in bone density in response to their training.  Martial artists who strike objects with increasing intensity (e.g., repeated elbow strikes), display increases in bone density in the striking area. This process is termed cortical remodeling
  • Frost’s Mechanostat Concept According to the Mechanostat, bone growth and bone loss is stimulated by the local mechanical elastic deformation of bone. The reason for the elastic deformation of bone is the peak forces caused by muscles The Adaptation of bone according to the maximum forces is considered to be a lifelong process. Hence bone adapts its mechanical properties according to the needed mechanical function – bone mass, bone geometry and hence bone strength is adapted according to the every-day usage / needs.
  • Frost’s Mechanostat Concept Strain : Deformation per unit length. It is a dimensionless parameter that is expressed as percent strain or micro strain. For instance, when a bone of 100 mm in length is elongated by 2 mm, the associated strain is expressed as 2% strain, 0.02 strain, or 20,000 micro strain. Normal=200-2500µ£=0.02%-0.25% Atrophy=<200µ£=<0.02% Hypertrophy =2500-4000µ£=0.25%-0.4% Fatigue failure=>4000µ£=>0.4% Spontaneous fracture=25000µ£=2.5% Ultimate strength of bone=25000µ£=2.5%
  • Benninghoff’s Stress Trajectories  It states that lines of orientation of bony trabeculae corresponds to the pathways of maximal pressure and tension that bony trabeculae are thicker in the region where the stress is greater.
  •  In Maxilla – frontonasal buttress, malar Zygomatic buttress,pterygoid buttress  In Mandible - Condyle, Gonial angles, Coronoid process
  • Modeling & Remodeling  The modern physiologic concept of bone remodeling is largely attributed to Harold Frost.  He differentiate Bone “modeling”(change in shape, size, and position of bones) FROM  Bone “remodeling”(coupled turnover sequence)
  • Modeling & Remodeling Both trabecular & cortical bone grow, adapt & turn over by means of these two fundamentally distinct mechanisms MODELING   Changes the shape, size, or position of bones in response to mechanical loading or wounding. Independent site of resorption & formation change the form of a bone. REMODELING  Physiologic term for  It is a coupled sequence of catabolic and anabolic events to support calcium homeostasis and repair / renew aged or damaged mineralized tissue. internal turnover of a mineralized tissue, without a change in its overall form.
  • Modeling & Remodeling Modeling Remodeling Independent site of resorption & formation change the form of a bone Specific coupled sequence of resorption & formation occurs to replace previously existing bone
  • An example of this process long bone increases in length and diameter. Bone modeling occurs during birth to adulthood and is responsible for gain in skeletal mass and changes in skeletal form. Dominant process of facial growth & adaptation to applied loads such as head gear, RPE, functional appliance. Changes can be seen on the ceph tracings. After peak bone mass has been approached, remodeling becomes the final common pathway by which bone mass is adjusted throughout adult life. Take place at the same time, but apparent only at the microscopic level . seen in bone scans and /or histology.
  • Modeling & Remodeling Where bone strains exceed bone's modeling threshold range, modeling can switch on to strengthen the bone. whereas when bone strains stay below a lower threshold range, disuse-mode remodeling can turn on to reduce whole bone strength by removing some trabecular and endocortical bone.
  • Growth factors that regulate bone remodelling 1. 2. 3. 4. Insulin – like growth factors (IGF) I & II Transforming growth factor –b (TGF – b) superfamily, including the bone morphogenetic proteins (BMPs) Fibroblast growth factors (FGF) Selected cytokines of the interleukin (IL), tumour necrosis factor (TNF), & colony – stimulating factor (CSF) families
  • REMODELING:  GOALS : • It provides a way for the body to alter the balance of essential minerals by increasing or decreasing the concentration of these in serum. • It provides a mechanism for the skeleton to adapt to its mechanical environment reducing risk to fracture
  • Basic multi-cellular unit (bmu) The process of bone resorption and formation are closely linked within discrete temporary anatomic structures called as „basic metabolizing units‟(by Frost)later called as basic multicellular unit They are readily present in cortical bone but there are evidence for the same concept in cancellous bone. The cellular components of a BMU maintains the same spatial & temporal relationship to each other while moving through or across the bone.
  • BASIC MULTICELLULAR UNIT
  • REMODELING IN CORTICAL BONE  Axially oriented cutting & filing cones are the mechanism underlying internal remodeling of dense compact bone.  The cutting/filling cone has a head of osteoclasts that cuts through the bone & a tail of osteoblasts that forms a new secondary osteon.  10 osteoclasts dig a circular tunnel osteoblasts that fill the tunnel .  It requires about 29 days to create resorption cavity (200-250µm in diameter) and 134 days to refill it .  Remodeling rate 2%-10% per year. followed by thousands of
  • REMODELING IN TRABECULAR BONE  Due to much larger surface to volume ratio it is more actively remodeled than cortical bone, with remodeling rate 10 times higher .  In trabecular bone 151days ; remodeling here is surface event.  Here osteoclasts digging a trench rather than tunnel and resulting structure that is formed is called a hemi cutting/filling cone .  Remodeling rate 20%-30% per year.
  • Hemi cutting/filling cone in showing the mechanism for coupling bone resorption to formation
  • Summary of remodelling process Micro cracks in bone causes Release of inflammatory cytokines cells(prostaglandins,interleukin) &exposure of mineralised collagen to extracellular fluid T- cells produce RANKL which induces osteoclasts histogenesis RANKL stimulates preosteoclasts from circulatory blood through RANKL receptors to form osteoclasts Bone resorption takes place Growth factors are produced & they stimulate preosteoclasts to produce OPG Mononuclear cells coat the irregular or scalloped resorbing surface with cementing surface Perivascular cells migrate & differentiate to preosteoblast Osteoblasts form new bone
  • Control of Remodeling   Two control loops regulate bone remodeling Homeostasis in the blood (negative feedback) Hormonal mechanism maintains calcium  Mechanical and gravitational forces acting on the skeleton
  • Hormonal Mechanism     Rising blood Ca2+ levels trigger the thyroid to release calcitonin Calcitonin inhibits bone resorption and stimulates calcium salt deposit in bone Falling blood Ca2+ levels signal the parathyroid glands to release parathyroid hormone (PTH) PTH signals osteoclasts to degrade bone matrix and release Ca2+ into the blood
  • Fracture & Repair of Bone Healing is faster in bone (vascular) than in cartilage (avascular) Repair is still slow due to BV damage Clinical treatment - closed reduction: restore pieces to normal position by manipulation - open reduction: realignment during surgery
  • Aging & Bone Tissue  The loss of Ca+2 from bone matrix (demineralization)  may result in osteoporosis  rapid in women age 40-45 ( when estrogen levels decrease )  begins after age 60 in men Decreased rate of protein synthesis less collagen production less growth hormone  brittle bones more likely to fracture
  • CONCLUSION  Bone physiologic concepts have important clinical applications in orthodontics & dentofacial orthopaedics  A detailed knowledge of the dynamic nature of bone physiology is important for successful orthodontic practice.  Mechanical adaptation of bone to forces used in Orthodontics is the physiologic basis of Orthodontics and dento-facial orthopedics.
  • REFRENCE: • Physiology- Robert M. Berne Fifth Edition • Physiology- sembulingam • Anatomy- gray’s anatomy • Craniofacial growth- Sridhar premkumar • Wikipedia, the free encyclopedia
  • THANK YOU