Bone physiology
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Bone physiology

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  • WOVEN BONE In contrast to mature bone, newly formed bone does not have lamellar structure. The bundles of collagen fibers run randomly and interlace with each other. Because of this, it is called woven bone. All newly formed bones are woven bone. It is later replaced by lamellar bone.

 Bone physiology Bone physiology Presentation Transcript

  • PRESENTEDBY – Dr.Pushkardwivedi PG 2ND YEAR DEPT. OF PROSTHODONTICS BONE PHYSIOLOGY
  • CONTENTS Introduction- Definition Function of bone Classification of bone Anatomy of bone Types of bone Composition Structure of alveolar process Ossification process Functional zone
  • Bone homeostasis Remodelling Repair of fracture bone Physiology of bone in complete denture Healing of extraction socket Bone in implants Bone substitute Osteoporosis Aging and bone tissue Conclusion References
  • INTRODUCTION Bone tissue forms most of the skeleton, the framework that supports and protects our organs and allows us to move. Strong but light weight, bone is a dynamic, ever changing tissue. Throughout life, it is continually being broken down and formed. Bone is of vital importance to the dentist. Orthodontists wish to understand and control resorption so that they can position individual teeth within alveolar bone. Oral surgeons have interest in bone diseases, as well as bone metabolism, to provide treatment of trauma and developmental defects. Periodontists tries to maintain the maximum amount of alveolar support around the roots of the teeth.
  • Prosthodontist wish to maintain and preserve the alveolar bone in edentulous and dentulous areas to provide support for dental prosthesis.  In Implantology available bone is particularly important and describes the external architecture or volume of the edentulous area considered for Implants. The density of available bone in an edentulous site is determining factor in treatment planning, implant design, surgical approach, healing time and initial progressive bone loading during prosthetic reconstruction.
  • DEFINITION Bone (osteon), according to Dorland’s medical dictionary: Any distinct piece of the osseous framework, or skeleton, of the body, called osseous tissue. According to GPT 8- The hard portion of the connective tissue which constitutes the majority of the skeleton; it consists of an inorganic or mineral component and an organic component (the matrix and cells); the matrix is composed of collaganous fibers and is impregnated with minerals, mainly calcium phosphate (approx. 85%) and calcium carbonate (approx. 10%), thus imparting the quality of rigidity—called also osseous tissue.
  • PHYSIOLOGY: FUNCTION OF BONE
  • CLASSIFICATION OF BONES: BY POSITION
  • CLASSIFICATION OF BONES: BY SHAPE 1) LONG BONES- • Longer than they are wide (e.g Humerus) • Consist of a long shaft with two bulky ends or extremities • Primarily compact bone but may have a large amount of spongy bone at the ends or extremities
  • 2)SHORT BONES- •Cube shaped bones of wrist & ankle •Consist mainly of spongy bone, which is covered by a thin layer of compact bone. •Bones that form within tendons(e.g Patella)
  • 3) FLAT BONES- •Thin, flattened and a bit curved (e.g sternum & most skull bones)
  • 4) IRREGULAR BONES- •Bones with complicated shapes (e.g vertebrae,hip bone,Maxilla & Mandible) •Primarily spongy bone that is covered with a thin layer of compact bone
  • CLASSIFICATION OF BONES: BY GROSS STRUCTURE Compact boneCompact bone Spongy boneSpongy bone BY DEVELOPMENT Membranous ( ectodermal) boneMembranous ( ectodermal) bone Cartilaginous ( endochondral ) boneCartilaginous ( endochondral ) bone
  • ANATOMY: STRUCTURE OF BONE A typical long bone consist of following Diaphysis Epiphysis Metaphysis Articular cartilage Periosteum Medullary or marrow cavity Endosteum
  • Structure of Short, Irregular, and Flat Bones Thin plates of periosteum-covered compact bone on the outside with endosteum-covered spongy bone (diploë) on the inside Have no diaphysis or epiphysis Contain bone marrow between the trabeculae
  • HISTOLOGY OF BONE TISSUE  Like other connective tissues, bone tissue contains an abundant matrix surrounding the cells. The matrix is about 25% water, 25% protein fibres and 50% mineral salts.  There are 4 types of cells4 types of cells in bone tissue.  Osteoprogenitor cellsOsteoprogenitor cells are unspecialized cells derived from mesenchyme, the tissue from which all connective tissues are derived. They undergo mitosis and develop into osteoblasts. They are found in the periosteum, endosteum and in canals that contains blood vessels.
  •  OsteoblastsOsteoblasts are the cells that form bone, but they have lost the ability to divide by mitosis. They secrete collagen and other organic components needed to build bone tissue. The differentiation of osteoproginitor cells into osteoblast is acclererated by some hormones and some bone proteins called Skeletal growth factors. Function-Function- 1)1) Role in formation of bone matrix 2) Role in calcification ( through the alkaline phosphatase enzymes) 3) Synthesis of proteins.
  •  Osteocytes-Osteocytes- these cells are concerned with maintenance of bone. Small flattened and rounded cells embedded in bone lacunae. Derived from mature Osteoblast. Function-Function- 1) Help to maintain the bone as living tissue because of there metabolic activity. 2) Maintain the exchange of calcium between the bone and ECF.
  •  Osteoclast-Osteoclast- Concerned with bone resorption. Giant phagocytic mutinuecleated cells found in the lacunae of bone matrix. Derived from hemopoietic stem cells via monocytes.( CFU-M) Function-Function- Responsible for bone resorption during bone remodelling. Synthesis and release of lysosomal enzymes necessary for bone resorption in to bone resorbing compartment.
  • When we examine the structure of any adult bone, we find that it is made up of layers or LAMELLAE. This kind of bone is called lamellar bone. LAMELLARBONE
  • Each lacuna contains 1 osteocyte. Spreading out from each lacuna there are fine canals or canaliculi that communicate with those from other lacunae. The lamellar appearance of bone depends mainly on the arrangement of collagen fibres. The fibres of one lamellus run parallel to each other.
  • In contrast to mature bone, newly formed bone does not have lamellar structure. The bundles of collagen fibers run randomly and interlace with each other. Because of this, it is called woven bone. All newly formed bones are woven bone. It is later replaced by lamellar bone. WOVEN BONE
  • COMPACT /CORTICAL BONE This type of bone is made up of lamellae, which are arranged in the form of concentric rings that surround a narrow HAVERSION CANAL present at the center of each ring. The blood vessels, lymphatic vessels and nerves from the periosteum penetrate the compact bone through PERFORATING (VOLKMANN’S) CANALS. The blood vessels and nerves of these canals connect with blood vessels and nerves of medullary cavity and periosteum and those of CENTRAL (HAVERSION) CANAL.
  • Interstitial lamellae Concentric lamellae
  • One haversion canal and the lamellae around it constitute a HAVERSION SYSTEM or OSTEON. The central canals run longitudinally through bone. Around the canals are CONCENTRIC LAMELLAE, rings of hard, calcified matrix. The area between osteons contains INTERSTITIAL LAMELLAE. They also have lacunae with osteocyte and canaliculi but their lamellae are usually not connected to the osteons.
  • In contrast to compact bone, spongy bone does not contain true osteons. It consists of lamellae arranged in an irregular latticework of thin plates of bone called trabeculae. The spaces between the trabeculae of some bones are filled with red marrow, which produce blood cells. SPONGY BONE orTRABECULARBONE orCANCELLOUS BONE
  • COMPOSITION OF BONE BoneBone Inorganic 65% Organic 35%Inorganic 65% Organic 35% (Primarily calcium phosphate which is present in form of Highly insoluble crystals of Collagen 88-89% Non collagen 11-12% Hydroxy apatite) Glycoprotein Proteoglycan Sialoproteins Lipids Collagen fibers provide bone with great tensile strength while Inorganic salts allow bone to withstand compression.
  • STRUCTURE OF ALVEOLARPROCESS It has 2 parts: 1.1. Alveolar bone properAlveolar bone proper — also called cribriform plate or lamina dura. has 2 layers of bone 2.2. Supporting alveolar boneSupporting alveolar bone Compact lamellar bone Layer of bundle bone------this is the layer that PDL fibres insert into. Cortical plate( compact lamellar bone)---- forms inner & outer plates. Spongy bone ( cancellated bone)--- fills in area b/w cortical plates of bone.
  • The cortical plates are thinner in the maxilla than in the mandible. They are thickest in premolar & molar region of the mandible, especially on buccal side. In the anterior region of both the jaws, supporting bone is very thin & no spongy bone is found here. Alveolar bone proper is fused to cortical plate. (This is seen esp. in mandibular incisor region. One or more roots may be partially or totally denuded of bone {fenestration or dehiscence} and these may have significance, if associated with alveolar bone loss due to chronic periodontal disease or if they occur in an area in which fixed bridge or denture abutment are contemplated)
  • The cortical bone acts as the primary stress bearing area in both maxillary and mandibular edentulous arches. In former it is the crest of residual alveolar ridge whereas in latter it is the buccal shelf area. These areas help in minimizing the vertical stresses produced by the prosthesis. Radiographically, spongiosa of the alveolar bone is of 2 main types. 1. Type I - Interdental & radicular trabeculae are regular and horizontal in a ladder-like arrangement. Found in mandible (fits well into general idea of a trajectory pattern of spongy bone) 2. Type II - Irregularly arranged, numerous, delicate interdental & radicular trabeculae. Found in maxilla (lacks trajectory pattern)
  • PHYSIOLOGY OF BONE FORMATION: OSSIFICATION The process by which bone forms is called OSSIFICATION. The skeleton of a human embryo is composed of fibrous connective tissue membrane formed by embryonic connective tissue (mesenchyme) and hyaline cartilage that are loosely shaped like bones. They provide supporting structure for ossification. Ossification begins around the 6th or 7th week of embryonic life and continues throughout adulthood.
  • Bone formation follows one of 2 patterns; 1. Intramembranous ossification- refers to the formation of bone directly on or within the fibrous connective tissue membranes. 2. Endochondral ossification- refers to the formation of bone in hyaline cartilage •Maxilla forms by intramembranous ossification. •Mandible forms partly by intramembranous and partly by intracartilaginous ossification. Greater part of body, ramus,condyloid and coronoid process are intramenbranous in origin. Only the tip of condyloid and coronoid process are of endochondral origin.
  • INTRAMEMBRANOUS OSSIFICATION 1)At the site where bone will develop, mesenchymal cells become vascularized, cluster and differentiate, First into osteoprogenitor cells and then into osteoblasts. The site of such a cluster is called a centre of ossification. Osteoblasts secrete the organic matrix of bone and gets surrounded to become osteocytes. Later calcium & other minerals are deposited and tissue calcifies
  • As the bone matrix forms, it develops into trabeculae. As trabeculae develop in various ossification centres, they fuse with one another to create the open latticework appearance of spongy bone. Connective tissue in trabecular spaces differentiates into red bone marrow. On the outside of bone, vascularized mesenchyme develops into periosteum. Eventually, Some of the spongy bone is replaced by the cortical bone. This will remodeled to reach its adult size & shape.
  • Begins in the second month of development Uses hyaline cartilage “bones” as models for bone construction Requires breakdown of hyaline cartilage prior to ossification ENDOCHONDRAL OSSIFICATION 1)1) Development of the cartilage model.Development of the cartilage model. • Mesenchymal cells differentiate into chondroblasts which form the hyaline cartilage model • A membrane called perichondrium develops around the cartilage
  • 2)Growth of the cartilage model2)Growth of the cartilage model •Cartilage model grows by interstitial & appositional growth •Chondrocytes in mid-region calcify the matrix •Vacated lacunae forms small cavities •Osteoblasts in perichondrium produce periosteal bone collar( once perichondrium starts to form bone, it is known as periosteum)
  • 3) Development of primary ossificationDevelopment of primary ossification centercenter •Near the middle of the model, capillaries of the periosteum grow into the disintegrating calcified cartilage. •These vessels and the osteoblasts, osteoclasts & red marrow cells, are known as the periosteal bud. •With the development of periosteal bud, primary ossification center and medullary cavity forms.
  • 4) Development of the diaphysis and epiphysisDevelopment of the diaphysis and epiphysis •The diaphysis, which was once a solid mass of hyaline cartilage, is replaced by compact bone. •When blood vessels( epiphyseal arteries) enter the epiphysis, secondary ossification centers develop. ( usually around the time of birth)
  • PHYSIOLOGY OF BONE GROWTH Bones grow in length at the epiphyseal plate by a process that is similar to endochondral ossification. The cartilage in the region of the epiphyseal plate next to the epiphysis continues to grow by mitosis. The chondrocytes, in the region next to the diaphysis, age and degenerate. Osteoblasts move in and ossify the matrix to form bone. This process continues throughout childhood and the adolescent years until the cartilage growth slows and finally stops. The epiphyseal plate completely ossifies so that only a thin epiphyseal line remains and the bones can no longer grow in length.
  • •Even though bones stop growing in length in early adulthood, they can continue to increase in thickness or diameter throughout life in response to stress from increased muscle activity or to weight. The increase in diameter is called appositional growth. •Osteoblasts in the periosteum form compact bone around the external bone surface. At the same time, osteoclasts in the endosteum break down bone on the internal bone surface, around the medullary cavity. These two processes together increase the diameter of the bone.
  • Growth zone – cartilage cells undergo mitosis, pushing the epiphysis away from the diaphysis Transformation zone – older cells enlarge, the matrix becomes calcified, cartilage cells die, and the matrix begins to deteriorate Osteogenic zone – new bone formation occurs Functional Zones in Long Bone Growth
  • BONE HOMEOSTASIS Bone, like skin, forms before birth but continually renews itself thereafter. REMODELING is the ongoing replacement of old bone tissue by new bone tissue. It takes place at different rates in various parts of body. OsteoclastsOsteoclasts are responsible for bone resorption (destruction of matrix). A delicate homeostasis exists between the actions of the osteoclasts in removing minerals and collagen and of osteoblasts in depositing them. A loss of too much calcium or tissue weakens the bones, and they break, as occurs in osteoporosisosteoporosis,, or become too flexible, as in osteomalacia.osteomalacia. Abnormal acceleration of remodeling process results in a condition called paget’s diseasepaget’s disease..
  • 1)1) ACTIVATIONACTIVATION- osteoclasts are activated & begin secreting acids to resorb bone. 2)2) RESORPTIONRESORPTION- osteoclastic resoprtion occurs. 3)3) REVERSALREVERSAL- resorption stops & osteoblast take over. 4)4) FORMATIONFORMATION- osteoblast form bone on the opposing surface to complete the bone reforming process. This cycle takes about 100 days in Compact bone & 200 days in Spongy bone. BONE REMODELING ( THE ARF CYCLE)
  • FirstFirst, Bone adjusts its strength in proportion to degree of bone stress. So the bones thicken when subjected to heavy loads. SecondSecond, even the shape of the bone can be rearranged for proper support of mechanical forces in accordance with stress patterns. ThirdThird, new organic matrix is needed as the old organic matrix degenerates. Value of continual bone remodeling
  • Long Bone Growth and Remodeling
  • Normal bone growth in the young and bone replacement in the adult depend on the presence of several minerals. Sufficient amount of calcium and phosphorus (component of hydroxy apatite), the primary salts that makes the bone matrix hard, must be included in the diet. Magnesium deficiency Inhibit the activity of osteoblasts Boron A factor in bone growth Manganese deficiency Inhibits laying down of new bone Tissue MINERALS NEEDEDFORBONE REMODELLING
  • Several vitamins like vitamins D, C, A, and B12, play a role in bone remodeling. The most active form of vitamin D is calcitriol. Acting as a hormone, it promotes removal of calcium from bone. On the other hand,it retards calcium loss in urine, which makes it available for deposit in bone matrix. Vit C deficiency causes decrease collagen production, which retards bone growth and delays fracture healing . Vit A helps to control the activity , distribution, and co-ordination of osteoblasts and osteoclasts during development. Its deficiency results in a decreased rate of growth in the skeleton. Vit B12 may play a role in osteoblast activity. VITAMINS NEEDEDFORBONE REMODELLING
  • HORMONES THAT EFFECT HOMEOSTASIS OF BONE TISSUE AND REMODELLING Hormone Function Human growth hormone (HGH) General growth of all body tissues, including bone Sex hormones ( estrogens and testosterones) Increase bone building activity of osteoblasts Insulin and thyroid hormones (T3, T4) Promote normal bone growth and maturity Parathyroid hormone Increase the number and activity of osteoclast,promotes recovery of Ca2+ from urine, and promotes formation of calcitriol Calcitonin (CT) Inhibits activity of osteoclasts, speed up Ca2+ absorption from blood, and accelerates Ca2+ deposit by bones.
  • Hormonal Regulation of Bone Growth During Youth During infancy and childhood- epiphyseal plate activity is stimulated by growth hormone During puberty- testosterone and estrogens: Initially promote adolescent growth spurts Cause masculinization and feminization of specific parts of the skeleton Later induce epiphyseal plate closure, ending longitudinal bone growth
  • BONE’S ROLE IN CALCIUM METABOLISM Some stimulus disrupts homeostasis by causing Decrease in ca2+ level Receptors Parathyroid gland cells detect lowered ca2+ conc Control center PTH gene turned on INPUT sed cAMP OUTPUT sed release of PTH Effector Osteoclast increase bone resorption Kidney release ca2+ in blood, excrete phosphate in urine, and produce calcitriol Response Increase in blood ca2+ level Return to homoestasis when response brings ca++ back to normal
  • Repair of bone after fracture
  • Physiology of Bone in complete denture •The reaction of bone to a change in function is subjected to the supreme test when the natural teeth are extracted and replaced with the dentures. •Wolff’s lawWolff’s law stated that a change in form follows a change in function owing to alteration of the internal architecture and external confirmation of the bone. Intermittent Stimulation Bone Apposition Constant stimulation Bone Resorption
  • NeufeldNeufeld reported that in some of the specimens studied, the trabecular pattern was arranged in such a way that it is dicated that there was some adaptation of the structure of the bones to the presence of an appliance in the region near the superior surfaces of the alveolar process It seems possible that the trabeculae pattern will arrange itself in such a manner that it will indicate resistance to the stress applied through such an appliance.
  • Reaction of bone to the pressure-Reaction of bone to the pressure- The continuous presence of dentures is capable of exerting pressure of sufficient intensity to produce resorption. This is particularly true in mandibular arch, since gravity exerts a steady pull on the dentures. When pressure diminishes the blood supply of bone tissue or interferes with its venous drainage, resorption results. A denture is potentially capable of exerting steady pressure and also intermittent heavy pressure that can interrupt the blood supply.
  • Healing of extraction socket- The removal of a tooth initiates the sequence of inflammation, epithelization, fibroplasia & remodeling. Socket heals by secondary intention & it takes minimum of 6 months for healing of a socket to the degree to which it becomes difficult to distinguish from the surrounding bone when viewed radiographically When a tooth is removed, the remaining empty socket consists of cortical bone (radiographic lamina dura) & a rim of oral epithelium left at the coronal portion.
  • In 30 minutes, the socket fills with blood, which coagulates & seals the socket from the oral environment. During the 1st week, inflammatory stage takes place.  All debris, bone fragments & contaminating bacteria will be removed by leukocytes  Fibroplasia begins with the ingrowth of fibroblasts & capillaries  Epithelium migrates along the inner surface until they meet or till the bed of granulation tissue  At the end of 1st week osteoclasts accumulate along the crestal bone.
  • During 2nd month, Histologically the socket is filled with immature bone by the end of second month and there is some quantitative loss when healing is uneventful. This loss in quantity during normal healing after extractions is one of the reasons of waiting period of 6 weeks to 2 months is often advocated prior to the placement of the dentures
  • During 4th – 6th month,  It is not until 4 – 6 months after extraction, the cortical bone lining a socket is fully resorbed, which is radiographically evident when there is loss of distinct lamina dura.  The epithelium moves towards the crest & eventually becomes level with the adjacent crestal gingiva.  At Ist year, the only remnants visible after 1 year is the rim of poorly vascularized fibrous tissue (scar) that remains on the edentulous ridge.
  • CHANGES IN THE SIZE OF BASAL SEAT Maxillary teeth generally flare downward and outward, so bone reduction generally is upward and inward. Since the outer cortical plate is thinner than the inner cortical plate, resorption from the outer cortex tends to be greater and more rapid. As the maxillary residual ridges are reduced, the maxillae become smaller in all dimensions and the denture-bearing surface decreases.
  • The anterior mandibular teeth generally incline upward and forward to the occlusal plane, whereas the posterior teeth are inclined slightly lingually. The outer cortex is generally thicker than the lingual cortex. Also, the width of the mandible is greatest at its inferior border. As a result, the mandibular residual ridge appears to migrate lingually and inferiorly in the anterior region and to migrate buccally in the posterior region. Consequently, the mandibular arch appears to become wider posteriorly as resorption progresses
  • Aristotle University Medical Journal, Vol. 33, Issue 2, 2006 Stage 1: preextraction, Stage 2: postextraction, Stage 3: high well-rounded ridge, Stage 4: knife-edge shaped ridge, Stage 5: low well-rounded ridge, Stage 6: depressed bone level. Classification systemof six atrophy stages in the maxilla (A) and the mandible (B) according to Atwood (1963)& Fallschussel(1986)
  • Procedures used in complete denture service to minimize the loss of alveolarbone include 1)Recording the tissues in the impression at their rest position. 2)Decreasing the number of teeth. 3)Decreasing the size of food table 4)Developing an occlusion that eliminates, as much as possible, horizontal forces and those that produces torque 5)Extending the denture bases for maximum coverage within tissue limits. 6)Eating by placing small masses of food over the posterior teeth where the supporting bone is best suited to resist force. 7)Removing the dentures for at least 8 of every 24 hours for tissue rest. 8) Regular follow-up.
  • Long term success rate in implant dentistry requires the evaluation of many criteria, many of which are unique to the discipline. However, the doctor’s training and experience and the amount and density of bone available bone in the edentulous site of the patient are arguable primary determining factors in predicting individual patient success Evaluation of bone in implants
  • In the past the available bone was not modified and was the primary intraoral factor influencing the treatment plan. Today the prosthetic needs and desire of the patient should be the first determined, relative to the number and position of missing teeth. After the intended prosthesis is designed, the patient force factor and bone density are evaluated. The key implant position , implant number and size are determined. After these factors are considered, the most important element in the implant region is the available bone .
  • BONE CLASSIFICATION SCHEMES RELATEDTO IMPLANT DENTISTRY
  • Lekholmand zarb (1985)classification- Composed of homogenous compact mass Thick layer of cortical bone surrounding dense trabeculae bone Thin layer of cortical bone surrounding dense trabeculae bone Thin layer of cortical bone surrounding a core of low-density trabeculae bone Found in the anterior region of jaw-Found in the anterior region of jaw-
  • Misch bone density classification scheme In 1988, Carl E. Misch proposed four bone density groups independent of the regions of the jaws, based on macroscopic cortical and trabecular bone characteristics. The region of the jaws with similar densities were often consistent. Dense or porous cortical bone is found on the outer surfaces of bone and includes the crest of an edentulous ridge. Coarse and fine trabecular bone types are found within the outer shell of cortical bone and occasionally on the crestal surface of an edentulous residual ridge.
  • Bone density Description Anatomical location D1 Dense cortical Anterior mandible D2 Porous cortical and coarse trabecular Anterior mandible, posterior mandible, anterior maxilla D3 Porous cortical(thin) and fine trabecular Anterior maxilla, posterior maxilla, posterior mandible D4 Fine trabecular Posterior maxilla
  • A key determinant for clinical success is the diagnosis of the bone density in a potential implant site. The strength, modulus of elasticity and percentage of bone- implant contact is related to the bone density and the axial stress contours around an implant are affected by density of bone. As a consequences, past clinical reports that did not alter the protocol of treatment related to bone density had variable survival rates. To the contrary, altering the treatment plan to compensate for soft bone types has provided similar survival rates in all the bone densities. The treatment plan may be modified by reducing the force on the prosthesis or increasing the area of load by increasing implant number, implant design, or implant body surface condition.
  • I) Bone graft materials AUTOGENOUS BONE GRAFTSAUTOGENOUS BONE GRAFTS a) Bone from intra-oral sites: osseous coagulum, bone blend, intra-oral cancellous bone marrow transplants, Bone swaging. b) Bone from extra-oral site: iliac autografts ALLOGRAFTS / HOMOGRAFTSALLOGRAFTS / HOMOGRAFTS a) Undecalcified freeze-dried bone allograft (FDBA) b) Decalcified freeze-dried bone allograft (DFDBA): bone morphogenic proteins BMP, osteogenin XENOGRAFTSXENOGRAFTS- Calf bone , inorganic bone BONE SUBSTITUTES
  • II) Non-bone graft materials • Sclera • Cartilage • Plaster of paris • Calcium phosphate biomaterials 2 types of calcium phosphate ceramics have been used: 1) hydroxy apatite 2) Tricalcium phosphate • Bioactive glass • Coral derived materials
  • It is the loss of bone mass & density throughout the body, including the jaws. The basic problem is that resorption outpaces bone formation. The common causes are: Lack of physical stress on bones. Malnutrition Lack of vitamin C Postmenopausal lack of estrogen secretion Old age Cushing syndrome OSTEOPOROSIS
  • Riggs & Menton (1998) distinguished two distinct syndromes of involutional osteoporosis. 1. Type1/postmenopausal osteoporosis: in which a loss of trabecular bone is predominant, resulting in fractures of vertebrae and wrist. 2. Type2/senile osteoporosis: in which both cortical and cancellous bone are lost, resulting in hip fractures as well.
  • TreatmentTreatment Adequate diet & exercise are the mainstays for preventing osteoporosis. In postmenopausal women, estrogen replacement therapy, Ca2+ supplements and weight bearing exercise help prevent osteoporosis
  • There are 2 principal effects of aging on bone tissue.  The first is the loss of calcium and other minerals from bone matrix (demineralization). This loss usually begins after age 30 in females, accelerates greatly around age 40 to 45 as levels of estrogen decrease, and continues until as much as 30% of calcium is lost by age 70. In males calcium loss does not begin until after age 60. The second principal effect of aging on the skeletal system is a decrease in the rate of protein synthesis. The bones become brittle and susceptible to fractures. AGING ANDBONE TISSUE
  • -Physiological principles govern all aspects of prosthodontic treatment and long term function. An understanding of the fundamental physiology, metabolism, and biomechanics of bone is essential for clinicians placing and restoring these devices. -With this knowledge of bone physiology, it is possible to institute procedures in prosthodontics that will assure a prosthesis which would be more acceptable to the patients. CONCLUSION
  • References- -Chaurasia B.D. Human antomy,5th edition. -Sembulingam K. essentials of medical physiology,4th edition -Guyton & Hall textbook of medical physiology,10th edition -Orban’s oral histology and embryology,10th edition -Winkler S. Essentials of complete denture prosthodontics,2nd edition -Heartwell C.M. Syllabus of Complete denture,4th edition - Peterson’s principles of oral & maxillofacial surgery,4th edition. -Misch C. E. contemporary implant dentistry,3rd edition:Elsevier -Ayse gulsahi Bone quality assessment for dental implants Khosla S. Rigg L. Pathophysiology of Age-Related Bone Loss and osteoporosisEndocrinol Metab Clin N Am 34 (2005) 1015–1030