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PHYSIOLOGY OF BONE
PRESENTED BY: Dr. Akanksha Narela
1ST YEAR PG
CONTENTS
PART-1
o Introduction
o Definition
o Function of bone
o Classification of bone
o Anatomy of bone
o Types of bone cells
o Types of bone
o Composition
o Structure of alveolar process
o Ossification process
o Functional zone
o Theories of bone
o Development of maxillae
o Development of mandible
o References
o Bone homeostasis
o Remodelling
o Factors affecting remodelling
o Repair of fracture bone
o Residual ridge resorption
o Prosthodonttics consideration
o Physiology of bone in complete denture
PART-2
o Healing of extraction socket
o Bone in implants
o Pathophysiology of bone
o Bone necrosis
o Aging and bone tissue
o Conclusion
o 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
Support
Protection
Movement
Mineral
homeostasis
Site of blood
cell
production
Storage of
energy
Classification of bone
According to position
 Axial skeleton
 Appendicular skeleton
According to development
 Membrane(dermal) bones
 Cartilaginous bones
 Membrano-cartilaginous bones
According to shape
 Long bones
 Short bones
 Flat bones
 Irregular bones
 Pneumatic bones
 Sesamoid bones
Structural classification
 Compact bones
 Cancellous spongy or trabecular bones
Classification Of Bones: By Position
 Axial skeleton – Bone forming axis of body. e.g Skull,
rib, sternum and vertebrae
 Appendicular skeleton –Bones forming appendages of
body e.g Bones of the limbs, shoulder, and hip
Classification Of Bones: By Shape
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
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)
FLAT BONES-
• Thin, flattened and a bit curved (e.g sternum & most
skull bones)
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
PNEUMATIC BONES-
 Irregular bones contain large air spaces lined by
epithelium
 Maxilla, sphenoid, ethmoid
SESAMOID BONES-
 Bony nodules embedded in tendons or joint capsules.
 Patella, fabella etc.
CLASSIFICATION OF BONES:
BY GROSS STRUCTURE
Compact Bone
 Solid bone,
 Dense in texture but porous
 Except for those accommodating cells,
processes and blood vessels
 Arms and legs
 Adaptation to bending and twisting
forces
Spongy bone
 Open in texture , meshwork of
trabeculae
 Usually interior of bone
 Many spaces between spicules (or
trabeculae) of bone
 Marrow found within the spaces
 Spine, ribs, jaw, wrist
 Adaptation of compressive forces
Classification Of Bones: By Development
Membranous ( ectodermal) bone
 Ossify in membrane – derived from intra membranous ossification
 Bones of vault of skull and facial bones
Cartilaginous ( endochondral ) bone
 Endochondral ossification
 Vertebral columns , thoracic cage, bones of limbs
Membrano-cartilaginous bones
 Clavicle, mandible, sphenoid, occipito temporal
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
Types of bone cells
 Osteoprogenitor – resting cell that can transform into an
osteoblast and secrete bone matrix
 Osteoblasts – Produces new bone, derived from bone
marrow cells
 Osteocytes – not clear, osteoblasts when they lose their
activity become osteocytes
 Osteoclasts – lyse or eat away bone, derived from
precursors of monocyte in the bone marrow
Osteoprogenitar cells
Appearance
• pale staining,
• small, spindle shaped
Location
• present on all non-resorbing surface
Function
• give rise to osteoblasts in vascularized regions
• chondroblasts in avascular regions
Osteoblasts
Appearance
• Large nondividing cells, eccentric nucleus,
basophilic cytoplasm, negative Golgi image,
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
• forms bone matrix in repair conditions.
• release calcium ions from bone matrix when
calcium demands increase
Osteoclast
Appearance
• multinucleated,
• non-dividing cells,
• very acidophilic.
• have a ruffled border and clear zone
Origin
• From blood monocytes/ macrophages
Osteoclast
Periosteum
• A thin connective tissue layer surrounding bone
• Contains the cells that are the source of bone
 Osteoprogenitor cells
• Must be preserved during surgery
At microscopic level, there are 4 types
of bone.
 Woven bone
 Lamellar bone
 Composite bone
 Bundle bone
( Contemporary implant dentistry , MISCH, 3rd edition)
LAMELLAR BONE
 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.
• 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.
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.
COMPACT /CORTICAL BONE
SPONGY BONE Or TRABECULAR BONE
Or CANCELLOUS BONE
• 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.
COMPOSITION OF BONE
Bone
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 ALVEOLAR PROCESS
 It has 2 parts:
1. Alveolar bone proper — also called cribriform plate or lamina dura.
2. Supporting alveolar 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.
Intramembranous
• Bone develops from fibrous
Membrane
• Forms bones of skull and clavicle (all
flat bones)
• Begins at 8 weeks of development
Endochondral
• Bone develops from hyaline cartilage
• Forms all bones below base of skull
• Begins 2nd month of development
INTRAMEMBRANOUS OSSIFICATION
Mesenchymal cells create
fibrous CT framework for
ossification
Some mesenchymal cells
differentiate into
osteoblasts in an
ossification center
Osteoblasts secrete bone matrix, osteoid
Mineralization and
calcification of osteoid
Trapped osteoblasts become
osteocytes
Osteoid accumulates in
between embryonic
blood vessels, creating
trabeculae of woven
bone.
Mesenchyme on bone
face condense and
differentiate into
periosteum
A bone collar of thickly woven osteoid
forms around trabeculae and ossifies
into compact bone
Spongy bone (diploë) cavities made
up of trabeculae fill with red marrow
created from vessels (vascular
tissue)
ENDOCHONDRAL OSSIFICATION
Growing taller throughout
childhood!
Growing Taller!
(A closer look at the epiphyseal plate)
Lots of activity!
• rapidly mitotic cartilage, lengthening bone; chondrocytes
form columns
• enlarging size of chondrocytes (hypertrophy)
• matrix of cartilage calcifies and cells die forming spiky
tips
•spiky calcified cartilage reshapes into spongy bone, converted
Functional Zones in Long Bone Growth
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
Blood & Nerve Supply of Bone
Mechanism Of Bone Growth
The changes that bone deposition and resorption can produce are,
a) Change in size
b) Change in shape
c) Change in proportion
d) Change in relationship of the bone with adjacent structures.
A combination of bone deposition and resorption resulting in a growth movement towards
the depositing surface is “cortical drift”
Theories Of Bone Growth
 GENETIC THEORY – growth is controlled by genetic influence.
 SUTURAL GROWTH THEORY (SICHER) – cranio facial growth occurs at the suture
 CARTILAGINOUS THEORY( JAMES SCOTT) – intrinsic growth controlling factors are
present in cartilage and periosteum with sutures being only secondary.
 THE FUNCTIONAL GROWTH MATRIX CONCEPT (MELVIN MOSS) – claims that the
origin, form, position, growth and maintenance of all skeletal tissues and organs are
always secondary, compensatory and necesssary responces to chronologically and
morphologically prior events / processes that occur in specifically related non skeletal
tissues, organs / functioning spaces.
 VAN LIMBORG’S THEORY (1970) – suggested the following 5 factors that he believed
controlled growth.
a) Intrinsic genetic factor
b) Local epigenetic factors
c) General epigenetic factors
d) Local environmental factors
e) General environmental factors
 ENLOW’S EXPANDING ‘V’ PRINCIPLE – the growth
movements and enlargements of these bones occurs
towards the wide end of ‘v’ as a result of differential
deposition and selective resorption of bone.
It occurs in a number of regions such as the
base of the mandible, mandible body, palate, ends of long
bones, etc.
Development Of Maxillae
Development Of Mandible
References
 Text book of medical physiology, Arthur.C.Guyton, 9th edition.
 Essentials of medical physiology, K.Sembulingam, 3rd edition.
 Physiology, Robert.M.Berne, 5th edition.
 Orthodontics, current principles and techniques, Thomas.M.Graber, 3rd edition.
 Orthodontics, the art and science, S.I.Bhalaji, 5th edition.
 The anatomical basis of medicine and surgery, Gray’s anatomy, Peter.L.William, 39th
edition.
 New atlas of human anatomy, Thomas.O.Mccracken. 2nd edition.
 Robbins and cotran basic pathology, kumar, cotran, robbins, 7th edition.
 Oral histology (development, structure and function) A.R.Ten cate, 6th edition.
 Oral anatomy, histology and embryology, B.K.B.Berkovitz,G.R.Holland, B.J.Moxham 4th edition.
 Clinical biochemistry , ALLAN GAW, ROBERT A. COWAN, DENIS ST.J.O’REILLY, MICHAEL J.
STEWART, JAMES SHEPHERD.
 Human Embryology, Inderbir Singh, 7th edition.
 Contemporary implant dentistry , misch, 3rd edition.
 Douglas C. Wendt, The degenerative denture ridge-Care and treatment,J. Prosthet Dent
1974;32,5:477-492. Dr. AJAY GUPTA, Dr. BHAWANA TIWARI, Dr. HEMANT GOEL, Dr HIMANSHU
SHEKHAWAT, RESIDUAL RIDGE RESORPTION : A REVIEW, Indian Journal of Dental Sciences,
march 2010 , vol 2 issue 2.
 H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture syndrome in senile
osteoporosis: A nutritional consequence?, journal of bone and mineral research
 David J. Baylink, Jon E. Wergedal, Kenji Yamamoto, and Eberhard Manzke, Systemic factors in alveolar bone
loss, J Prosthet Dent. 1974;31,5:486-505.
 Atwood, DA. Some, clinical factors related to rate of resorption of residual ridges. J Pros Dent 1962; 12:441-50.
TO BE CONTINUED..
PHYSIOLOGY OF BONE
PRESENTED BY: Dr. Akanksha Narela
1ST YEAR PG
o Bone homeostasis
o Remodelling
o Factors affecting remodelling
o Repair of fracture bone
o Prosthodonttics consideration
o Physiology of bone in complete denture
o Healing of extraction socket
o Bone in implants
o Pathophysiology of bone
o Bone necrosis
o Aging and bone tissue
o Conclusion
o References
PART-2
CONTENT
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.
Osteoclasts 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
osteoporosis, or become too flexible, as in osteomalacia.
Abnormal acceleration of remodeling process results in a condition called paget’s disease.
BONE REMODELING ( THE ARF CYCLE)
ACTIVATION- osteoclasts are activated & begin secreting acids to resorb bone.
RESORPTION- osteoclastic resoprtion occurs.
REVERSAL- resorption stops & osteoblast take over.
FORMATION- 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.
Value Of Continual Bone Remodeling
First, Bone adjusts its strength in proportion to degree of bone stress. So the
bones thicken when subjected to heavy loads.
Second, even the shape of the bone can be rearranged for proper support of
mechanical forces in accordance with stress patterns.
Third, new organic matrix is needed as the old organic matrix degenerates.
Long Bone Growth and Remodeling
Factors Affecting Bone Growth
• - Ca & P for bone growth
• - vitamin C for collagen synthesis
• - vitamins K & B12 for protein synthesis
Nutrition: need
adequate levels of
minerals & vitamins
• - Insulin like 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
Need adequate
levels of specific
hormones
Minerals Needed For Bone Remodelling
• 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
VITAMINS NEEDED FOR BONE 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.
HORMONES THAT EFFECT HOMEOSTASIS OF
BONE TISSUE AND REMODELLING
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
Repair Of Bone After Fracture
Prosthodontic Considerations
DEFINITION
 Alveolar bone – “ The bony portion of the mandible or maxillae in which the roots of the
teeth are held by fibers of the periodontal ligament ”.(GPT- 8)
 Residual ridge resorption – A term used for the diminishing quantity and quality of the
residual ridge after teeth are removed. (GPT – 8)
Bone Substitutes
BONE GRAFT MATERIALS
 AUTOGENOUS BONE GRAFTS
 Bone from intra-oral sites: osseous coagulum, bone blend, intra-oral cancellous bone marrow transplants,bone
swaging.
 Bone from extra-oral site: iliac autografts
 ALLOGRAFTS
 Undecalcified freeze-dried bone allograft (FDBA)
 Decalcified freeze-dried bone allograft (DFDBA): bone morphogenic proteins BMP, osteogenin
 XENOGRAFTS
 Calf bone ,keil bone, anorganic bone
II) Non-bone graft materials
• Sclera
• Cartilage
• Plaster of paris
• Calcium phosphate biomaterials
2 types of calcium phosphate ceramics have been used:
 Hydroxy apatite
 Tricalcium phosphate
• Bioactive glass
• Coral derived materials
Residual Bone And Maxillomandibular Relation
 It is generally agreed that residual edentulous alveolar ridges resorb; however there remains
some controversy regarding the effect of dentures on the process.
 Some authorities discussed the concept of disuse atrophy and recommended that dentures
be constructed and worn to preserve the alveolar ridge. In contrast, others have
emphasized the mechanical trauma that is associated with the wearing of complete
dentures
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 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
• Neufeld reported that in some of the specimens studied, the trabecular pattern was
arranged in such a way that it is dictated 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-
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
4 Clinical Factors Related To Resorption
Rate :
Anatomic factors comprise size, shape, and density of ridges, thickness and character of
mucosal tissue, the ridge relationship, and number and depth of sockets. Resorption rate of
residual ridges depend on bone volume and bone density.
Metabolic factors - nutritional, hormonal, other metabolic factors that influence the
osteoblasts and osteoclasts activity.
Functional factors - consist of frequency, intensity, duration, and direction of force which
translated into biologic cell activity. Bone formation or bone resorption may result.
Prosthetic factors - technique, materials, concepts, principles and practices .
Procedures used in complete denture service
to minimize the loss of alveolar bone include
Recording the tissues in the impression at their rest position.
Decreasing the number of teeth.
Decreasing the size of food table
Developing an occlusion that eliminates, as much as possible, horizontal forces and those that
produces torque
Extending the denture bases for maximum coverage within tissue limits.
Eating by placing small masses of food over the posterior teeth where the supporting bone is best suited
to resist force.
Removing the dentures for at least 8 of every 24 hours for tissue rest.
Regular follow-up.
Evaluation Of Bone In Implants
• 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
• 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
RELATED TO IMPLANT DENTISTRY
Linkow (1970) classified BONE DENSITY into 3 categories;
Class I bone structure: This ideal bone type consists of evenly spaced trabeculae with
small cancellated spaces. (Very satisfactory foundation for implant prosthesis)
Class II bone structure: The bone has slightly larger cancellated spaces with less
uniformity of the osseous pattern. (Satisfactory for implants)
Class III bone structure: Large marrow-filled spaces exist between bone trabeculae.
(Results in loose fitting implants)
Lekholm and 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-
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.
• A key determinant for clinical success is the diagnosis of the bone density in a potential
implant site.
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
• 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.
PATHOPHYIOLOGY OF BONE
REMODELING
Bone Disease In Hyperparathyroidism
• In mild hyperparathyroidism bone can be deposited rapidly enough
• In severe hyperparathyroidism the bone may be eaten away almost entirely
• Radiograph shows extensive decalcification and large punched out cystic areas of the bone
that are filled with osteoclasts in the form of so called giant cell osteoclast tumors
• Multiple fractures of the weakened bones from slight trauma
• The cystic bone disease of hyperparathyroidism is called osteitis fibrosa cystica
• Large quantities of plasma alkaline phosphatase – due to osteoblastic activity
Rickets
• In prolonged case , the compensatory increase in PTH secretion
causes extreme osteoclastic absorption of the bone
• Bone becomes weaker and imposes marked physical stress on the
bone resulting in rapid osteoblastic activity
• These laid down large quantities of osteoid which does not become
calcified
Osteomalacia
• Deficiencies of vitamin D and calcium occur as a result of
steatorrhea
• Poor absorption of calcium and phosphate
• This almost never proceeds to the stage of tetany but often
is a cause of severe bone disability
OSTEOPOROSIS
• It is the loss of bone mass & density throughout the body, including the jaws.
• The basic problem is that resorption outpaces bone formation
 Lack of physical stress on bones.
 Malnutrition
 Lack of vitamin C
 Postmenopausal lack of estrogen secretion
 Old age
 Cushing syndrome
 Riggs & Ganguly (1991) 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.
B. LAWRENCE RIGGS , CONSTANTINOS D. CONSTANTINOU, LARISA SEREDA, ARUPA GANGULY, Mutation in a gene for type I procollagen (COL1A2) in a woman with
postmenopausal osteoporosis, Proc. Natl. Acad. Sci. USA Vol. 88, pp. 5423-5427, June 1991
Prevention Of Senile Osteoporosis
 Men – physical activity, exposed to sun light, adequate amount of calcium containing foods
or medicinal forms of calcium.
 Women – estrogen therapy, vitamin D supplements, use of fluorides, increased calcium
intake.
(H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture syndrome in senile osteoporosis: A nutritional
consequence?, journal of bone and mineral research )
AGING AND BONE TISSUE
 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.
CONCLUSION
• 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.
References
 Text book of medical physiology, Arthur.C.Guyton, 9th edition.
 Essentials of medical physiology, K.Sembulingam, 3rd edition.
 Physiology, Robert.M.Berne, 5th edition.
 Orthodontics, current principles and techniques, Thomas.M.Graber, 3rd edition.
 Orthodontics, the art and science, S.I.Bhalaji, 5th edition.
 The anatomical basis of medicine and surgery, Gray’s anatomy, Peter.L.William, 39th
edition.
 New atlas of human anatomy, Thomas.O.Mccracken. 2nd edition.
 Robbins and cotran basic pathology, kumar, cotran, robbins, 7th edition.
 Oral histology (development, structure and function) A.R.Ten cate, 6th edition.
 Oral anatomy, histology and embryology, B.K.B.Berkovitz,G.R.Holland, B.J.Moxham 4th edition.
 Clinical biochemistry , ALLAN GAW, ROBERT A. COWAN, DENIS ST.J.O’REILLY, MICHAEL J.
STEWART, JAMES SHEPHERD.
 Human Embryology, Inderbir Singh, 7th edition.
 Contemporary implant dentistry , misch, 3rd edition.
 Douglas C. Wendt, The degenerative denture ridge-Care and treatment,J. Prosthet Dent
1974;32,5:477-492. Dr. AJAY GUPTA, Dr. BHAWANA TIWARI, Dr. HEMANT GOEL, Dr HIMANSHU
SHEKHAWAT, RESIDUAL RIDGE RESORPTION : A REVIEW, Indian Journal of Dental Sciences,
march 2010 , vol 2 issue 2.
 H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture syndrome in senile
osteoporosis: A nutritional consequence?, journal of bone and mineral research
 David J. Baylink, Jon E. Wergedal, Kenji Yamamoto, and Eberhard Manzke, Systemic factors in alveolar bone
loss, J Prosthet Dent. 1974;31,5:486-505.
 Atwood, DA. Some, clinical factors related to rate of resorption of residual ridges. J Pros Dent 1962; 12:441-50.
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2.PHYSIOLOGY OF BONE.pptx

  • 1. PHYSIOLOGY OF BONE PRESENTED BY: Dr. Akanksha Narela 1ST YEAR PG
  • 2. CONTENTS PART-1 o Introduction o Definition o Function of bone o Classification of bone o Anatomy of bone o Types of bone cells o Types of bone o Composition o Structure of alveolar process o Ossification process o Functional zone o Theories of bone o Development of maxillae o Development of mandible o References
  • 3. o Bone homeostasis o Remodelling o Factors affecting remodelling o Repair of fracture bone o Residual ridge resorption o Prosthodonttics consideration o Physiology of bone in complete denture PART-2 o Healing of extraction socket o Bone in implants o Pathophysiology of bone o Bone necrosis o Aging and bone tissue o Conclusion o References
  • 4. 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.
  • 5.  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.
  • 6. 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.
  • 7. PHYSIOLOGY: FUNCTION OF BONE Support Protection Movement Mineral homeostasis Site of blood cell production Storage of energy
  • 8. Classification of bone According to position  Axial skeleton  Appendicular skeleton According to development  Membrane(dermal) bones  Cartilaginous bones  Membrano-cartilaginous bones According to shape  Long bones  Short bones  Flat bones  Irregular bones  Pneumatic bones  Sesamoid bones Structural classification  Compact bones  Cancellous spongy or trabecular bones
  • 9. Classification Of Bones: By Position  Axial skeleton – Bone forming axis of body. e.g Skull, rib, sternum and vertebrae  Appendicular skeleton –Bones forming appendages of body e.g Bones of the limbs, shoulder, and hip
  • 10. Classification Of Bones: By Shape 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
  • 11. 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)
  • 12. FLAT BONES- • Thin, flattened and a bit curved (e.g sternum & most skull bones)
  • 13. 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
  • 14. PNEUMATIC BONES-  Irregular bones contain large air spaces lined by epithelium  Maxilla, sphenoid, ethmoid
  • 15. SESAMOID BONES-  Bony nodules embedded in tendons or joint capsules.  Patella, fabella etc.
  • 16. CLASSIFICATION OF BONES: BY GROSS STRUCTURE Compact Bone  Solid bone,  Dense in texture but porous  Except for those accommodating cells, processes and blood vessels  Arms and legs  Adaptation to bending and twisting forces Spongy bone  Open in texture , meshwork of trabeculae  Usually interior of bone  Many spaces between spicules (or trabeculae) of bone  Marrow found within the spaces  Spine, ribs, jaw, wrist  Adaptation of compressive forces
  • 17. Classification Of Bones: By Development Membranous ( ectodermal) bone  Ossify in membrane – derived from intra membranous ossification  Bones of vault of skull and facial bones Cartilaginous ( endochondral ) bone  Endochondral ossification  Vertebral columns , thoracic cage, bones of limbs Membrano-cartilaginous bones  Clavicle, mandible, sphenoid, occipito temporal
  • 18. ANATOMY: STRUCTURE OF BONE A typical long bone consist of following Diaphysis Epiphysis Metaphysis Articular cartilage Periosteum Medullary or marrow cavity Endosteum
  • 19. 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
  • 20. Types of bone cells  Osteoprogenitor – resting cell that can transform into an osteoblast and secrete bone matrix  Osteoblasts – Produces new bone, derived from bone marrow cells  Osteocytes – not clear, osteoblasts when they lose their activity become osteocytes  Osteoclasts – lyse or eat away bone, derived from precursors of monocyte in the bone marrow
  • 21. Osteoprogenitar cells Appearance • pale staining, • small, spindle shaped Location • present on all non-resorbing surface Function • give rise to osteoblasts in vascularized regions • chondroblasts in avascular regions
  • 22. Osteoblasts Appearance • Large nondividing cells, eccentric nucleus, basophilic cytoplasm, negative Golgi image, cytoplasmic processes. Function • Synthesize and secrete organic constituents of bone matrix (osteoid) • aid in calcification.
  • 23. Osteocyte Appearance • smaller and less basophilic than osteoblast, • have interconnecting processes Function • forms bone matrix in repair conditions. • release calcium ions from bone matrix when calcium demands increase
  • 24. Osteoclast Appearance • multinucleated, • non-dividing cells, • very acidophilic. • have a ruffled border and clear zone Origin • From blood monocytes/ macrophages Osteoclast
  • 25. Periosteum • A thin connective tissue layer surrounding bone • Contains the cells that are the source of bone  Osteoprogenitor cells • Must be preserved during surgery
  • 26. At microscopic level, there are 4 types of bone.  Woven bone  Lamellar bone  Composite bone  Bundle bone ( Contemporary implant dentistry , MISCH, 3rd edition)
  • 27. LAMELLAR BONE  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.
  • 28. • 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.
  • 29. 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.
  • 31. SPONGY BONE Or TRABECULAR BONE Or CANCELLOUS BONE • 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.
  • 32. COMPOSITION OF BONE Bone 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.
  • 33. STRUCTURE OF ALVEOLAR PROCESS  It has 2 parts: 1. Alveolar bone proper — also called cribriform plate or lamina dura. 2. Supporting alveolar bone
  • 34.  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.
  • 35.  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.
  • 36.  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)
  • 37. 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.
  • 38. Intramembranous • Bone develops from fibrous Membrane • Forms bones of skull and clavicle (all flat bones) • Begins at 8 weeks of development Endochondral • Bone develops from hyaline cartilage • Forms all bones below base of skull • Begins 2nd month of development
  • 39. INTRAMEMBRANOUS OSSIFICATION Mesenchymal cells create fibrous CT framework for ossification Some mesenchymal cells differentiate into osteoblasts in an ossification center Osteoblasts secrete bone matrix, osteoid
  • 40. Mineralization and calcification of osteoid Trapped osteoblasts become osteocytes
  • 41. Osteoid accumulates in between embryonic blood vessels, creating trabeculae of woven bone. Mesenchyme on bone face condense and differentiate into periosteum
  • 42. A bone collar of thickly woven osteoid forms around trabeculae and ossifies into compact bone Spongy bone (diploë) cavities made up of trabeculae fill with red marrow created from vessels (vascular tissue)
  • 45. Growing Taller! (A closer look at the epiphyseal plate) Lots of activity!
  • 46. • rapidly mitotic cartilage, lengthening bone; chondrocytes form columns • enlarging size of chondrocytes (hypertrophy) • matrix of cartilage calcifies and cells die forming spiky tips •spiky calcified cartilage reshapes into spongy bone, converted
  • 47. Functional Zones in Long Bone Growth 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
  • 48. Blood & Nerve Supply of Bone
  • 49. Mechanism Of Bone Growth The changes that bone deposition and resorption can produce are, a) Change in size b) Change in shape c) Change in proportion d) Change in relationship of the bone with adjacent structures. A combination of bone deposition and resorption resulting in a growth movement towards the depositing surface is “cortical drift”
  • 50. Theories Of Bone Growth  GENETIC THEORY – growth is controlled by genetic influence.  SUTURAL GROWTH THEORY (SICHER) – cranio facial growth occurs at the suture  CARTILAGINOUS THEORY( JAMES SCOTT) – intrinsic growth controlling factors are present in cartilage and periosteum with sutures being only secondary.
  • 51.  THE FUNCTIONAL GROWTH MATRIX CONCEPT (MELVIN MOSS) – claims that the origin, form, position, growth and maintenance of all skeletal tissues and organs are always secondary, compensatory and necesssary responces to chronologically and morphologically prior events / processes that occur in specifically related non skeletal tissues, organs / functioning spaces.
  • 52.  VAN LIMBORG’S THEORY (1970) – suggested the following 5 factors that he believed controlled growth. a) Intrinsic genetic factor b) Local epigenetic factors c) General epigenetic factors d) Local environmental factors e) General environmental factors
  • 53.  ENLOW’S EXPANDING ‘V’ PRINCIPLE – the growth movements and enlargements of these bones occurs towards the wide end of ‘v’ as a result of differential deposition and selective resorption of bone. It occurs in a number of regions such as the base of the mandible, mandible body, palate, ends of long bones, etc.
  • 56. References  Text book of medical physiology, Arthur.C.Guyton, 9th edition.  Essentials of medical physiology, K.Sembulingam, 3rd edition.  Physiology, Robert.M.Berne, 5th edition.  Orthodontics, current principles and techniques, Thomas.M.Graber, 3rd edition.  Orthodontics, the art and science, S.I.Bhalaji, 5th edition.  The anatomical basis of medicine and surgery, Gray’s anatomy, Peter.L.William, 39th edition.  New atlas of human anatomy, Thomas.O.Mccracken. 2nd edition.  Robbins and cotran basic pathology, kumar, cotran, robbins, 7th edition.  Oral histology (development, structure and function) A.R.Ten cate, 6th edition.
  • 57.  Oral anatomy, histology and embryology, B.K.B.Berkovitz,G.R.Holland, B.J.Moxham 4th edition.  Clinical biochemistry , ALLAN GAW, ROBERT A. COWAN, DENIS ST.J.O’REILLY, MICHAEL J. STEWART, JAMES SHEPHERD.  Human Embryology, Inderbir Singh, 7th edition.  Contemporary implant dentistry , misch, 3rd edition.  Douglas C. Wendt, The degenerative denture ridge-Care and treatment,J. Prosthet Dent 1974;32,5:477-492. Dr. AJAY GUPTA, Dr. BHAWANA TIWARI, Dr. HEMANT GOEL, Dr HIMANSHU SHEKHAWAT, RESIDUAL RIDGE RESORPTION : A REVIEW, Indian Journal of Dental Sciences, march 2010 , vol 2 issue 2.  H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture syndrome in senile osteoporosis: A nutritional consequence?, journal of bone and mineral research
  • 58.  David J. Baylink, Jon E. Wergedal, Kenji Yamamoto, and Eberhard Manzke, Systemic factors in alveolar bone loss, J Prosthet Dent. 1974;31,5:486-505.  Atwood, DA. Some, clinical factors related to rate of resorption of residual ridges. J Pros Dent 1962; 12:441-50.
  • 60. PHYSIOLOGY OF BONE PRESENTED BY: Dr. Akanksha Narela 1ST YEAR PG
  • 61. o Bone homeostasis o Remodelling o Factors affecting remodelling o Repair of fracture bone o Prosthodonttics consideration o Physiology of bone in complete denture o Healing of extraction socket o Bone in implants o Pathophysiology of bone o Bone necrosis o Aging and bone tissue o Conclusion o References PART-2 CONTENT
  • 62. 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. Osteoclasts 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 osteoporosis, or become too flexible, as in osteomalacia. Abnormal acceleration of remodeling process results in a condition called paget’s disease.
  • 63. BONE REMODELING ( THE ARF CYCLE) ACTIVATION- osteoclasts are activated & begin secreting acids to resorb bone. RESORPTION- osteoclastic resoprtion occurs. REVERSAL- resorption stops & osteoblast take over. FORMATION- 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.
  • 64.
  • 65. Value Of Continual Bone Remodeling First, Bone adjusts its strength in proportion to degree of bone stress. So the bones thicken when subjected to heavy loads. Second, even the shape of the bone can be rearranged for proper support of mechanical forces in accordance with stress patterns. Third, new organic matrix is needed as the old organic matrix degenerates.
  • 66. Long Bone Growth and Remodeling
  • 67. Factors Affecting Bone Growth • - Ca & P for bone growth • - vitamin C for collagen synthesis • - vitamins K & B12 for protein synthesis Nutrition: need adequate levels of minerals & vitamins • - Insulin like 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 Need adequate levels of specific hormones
  • 68. Minerals Needed For Bone Remodelling • 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
  • 69. VITAMINS NEEDED FOR BONE 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.
  • 70. HORMONES THAT EFFECT HOMEOSTASIS OF BONE TISSUE AND REMODELLING
  • 71. 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
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  • 81. Repair Of Bone After Fracture
  • 82. Prosthodontic Considerations DEFINITION  Alveolar bone – “ The bony portion of the mandible or maxillae in which the roots of the teeth are held by fibers of the periodontal ligament ”.(GPT- 8)  Residual ridge resorption – A term used for the diminishing quantity and quality of the residual ridge after teeth are removed. (GPT – 8)
  • 83. Bone Substitutes BONE GRAFT MATERIALS  AUTOGENOUS BONE GRAFTS  Bone from intra-oral sites: osseous coagulum, bone blend, intra-oral cancellous bone marrow transplants,bone swaging.  Bone from extra-oral site: iliac autografts  ALLOGRAFTS  Undecalcified freeze-dried bone allograft (FDBA)  Decalcified freeze-dried bone allograft (DFDBA): bone morphogenic proteins BMP, osteogenin  XENOGRAFTS  Calf bone ,keil bone, anorganic bone
  • 84. II) Non-bone graft materials • Sclera • Cartilage • Plaster of paris • Calcium phosphate biomaterials 2 types of calcium phosphate ceramics have been used:  Hydroxy apatite  Tricalcium phosphate • Bioactive glass • Coral derived materials
  • 85. Residual Bone And Maxillomandibular Relation  It is generally agreed that residual edentulous alveolar ridges resorb; however there remains some controversy regarding the effect of dentures on the process.  Some authorities discussed the concept of disuse atrophy and recommended that dentures be constructed and worn to preserve the alveolar ridge. In contrast, others have emphasized the mechanical trauma that is associated with the wearing of complete dentures
  • 86. 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 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
  • 87. • Neufeld reported that in some of the specimens studied, the trabecular pattern was arranged in such a way that it is dictated 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.
  • 88. 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.
  • 89. 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.
  • 90. 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.
  • 91.  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
  • 92. 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.
  • 93. 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.
  • 94. 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
  • 95. 4 Clinical Factors Related To Resorption Rate : Anatomic factors comprise size, shape, and density of ridges, thickness and character of mucosal tissue, the ridge relationship, and number and depth of sockets. Resorption rate of residual ridges depend on bone volume and bone density. Metabolic factors - nutritional, hormonal, other metabolic factors that influence the osteoblasts and osteoclasts activity. Functional factors - consist of frequency, intensity, duration, and direction of force which translated into biologic cell activity. Bone formation or bone resorption may result. Prosthetic factors - technique, materials, concepts, principles and practices .
  • 96. Procedures used in complete denture service to minimize the loss of alveolar bone include Recording the tissues in the impression at their rest position. Decreasing the number of teeth. Decreasing the size of food table Developing an occlusion that eliminates, as much as possible, horizontal forces and those that produces torque Extending the denture bases for maximum coverage within tissue limits. Eating by placing small masses of food over the posterior teeth where the supporting bone is best suited to resist force. Removing the dentures for at least 8 of every 24 hours for tissue rest. Regular follow-up.
  • 97. Evaluation Of Bone In Implants • 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
  • 98. • 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
  • 99. BONE CLASSIFICATION SCHEMES RELATED TO IMPLANT DENTISTRY
  • 100. Linkow (1970) classified BONE DENSITY into 3 categories; Class I bone structure: This ideal bone type consists of evenly spaced trabeculae with small cancellated spaces. (Very satisfactory foundation for implant prosthesis) Class II bone structure: The bone has slightly larger cancellated spaces with less uniformity of the osseous pattern. (Satisfactory for implants) Class III bone structure: Large marrow-filled spaces exist between bone trabeculae. (Results in loose fitting implants)
  • 101. Lekholm and 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-
  • 102. 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. • A key determinant for clinical success is the diagnosis of the bone density in a potential implant site.
  • 103. 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
  • 104. • 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.
  • 106.
  • 107. Bone Disease In Hyperparathyroidism • In mild hyperparathyroidism bone can be deposited rapidly enough • In severe hyperparathyroidism the bone may be eaten away almost entirely • Radiograph shows extensive decalcification and large punched out cystic areas of the bone that are filled with osteoclasts in the form of so called giant cell osteoclast tumors • Multiple fractures of the weakened bones from slight trauma • The cystic bone disease of hyperparathyroidism is called osteitis fibrosa cystica • Large quantities of plasma alkaline phosphatase – due to osteoblastic activity
  • 108. Rickets • In prolonged case , the compensatory increase in PTH secretion causes extreme osteoclastic absorption of the bone • Bone becomes weaker and imposes marked physical stress on the bone resulting in rapid osteoblastic activity • These laid down large quantities of osteoid which does not become calcified
  • 109. Osteomalacia • Deficiencies of vitamin D and calcium occur as a result of steatorrhea • Poor absorption of calcium and phosphate • This almost never proceeds to the stage of tetany but often is a cause of severe bone disability
  • 110. OSTEOPOROSIS • It is the loss of bone mass & density throughout the body, including the jaws. • The basic problem is that resorption outpaces bone formation  Lack of physical stress on bones.  Malnutrition  Lack of vitamin C  Postmenopausal lack of estrogen secretion  Old age  Cushing syndrome
  • 111.  Riggs & Ganguly (1991) 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. B. LAWRENCE RIGGS , CONSTANTINOS D. CONSTANTINOU, LARISA SEREDA, ARUPA GANGULY, Mutation in a gene for type I procollagen (COL1A2) in a woman with postmenopausal osteoporosis, Proc. Natl. Acad. Sci. USA Vol. 88, pp. 5423-5427, June 1991
  • 112. Prevention Of Senile Osteoporosis  Men – physical activity, exposed to sun light, adequate amount of calcium containing foods or medicinal forms of calcium.  Women – estrogen therapy, vitamin D supplements, use of fluorides, increased calcium intake. (H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture syndrome in senile osteoporosis: A nutritional consequence?, journal of bone and mineral research )
  • 113. AGING AND BONE TISSUE  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.
  • 114. CONCLUSION • 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.
  • 115. References  Text book of medical physiology, Arthur.C.Guyton, 9th edition.  Essentials of medical physiology, K.Sembulingam, 3rd edition.  Physiology, Robert.M.Berne, 5th edition.  Orthodontics, current principles and techniques, Thomas.M.Graber, 3rd edition.  Orthodontics, the art and science, S.I.Bhalaji, 5th edition.  The anatomical basis of medicine and surgery, Gray’s anatomy, Peter.L.William, 39th edition.  New atlas of human anatomy, Thomas.O.Mccracken. 2nd edition.  Robbins and cotran basic pathology, kumar, cotran, robbins, 7th edition.  Oral histology (development, structure and function) A.R.Ten cate, 6th edition.
  • 116.  Oral anatomy, histology and embryology, B.K.B.Berkovitz,G.R.Holland, B.J.Moxham 4th edition.  Clinical biochemistry , ALLAN GAW, ROBERT A. COWAN, DENIS ST.J.O’REILLY, MICHAEL J. STEWART, JAMES SHEPHERD.  Human Embryology, Inderbir Singh, 7th edition.  Contemporary implant dentistry , misch, 3rd edition.  Douglas C. Wendt, The degenerative denture ridge-Care and treatment,J. Prosthet Dent 1974;32,5:477-492. Dr. AJAY GUPTA, Dr. BHAWANA TIWARI, Dr. HEMANT GOEL, Dr HIMANSHU SHEKHAWAT, RESIDUAL RIDGE RESORPTION : A REVIEW, Indian Journal of Dental Sciences, march 2010 , vol 2 issue 2.  H. Rico, M. Revilla, L. F. Villa, E. R. Hernandez, J. P. Fernandez, Crush fracture syndrome in senile osteoporosis: A nutritional consequence?, journal of bone and mineral research
  • 117.  David J. Baylink, Jon E. Wergedal, Kenji Yamamoto, and Eberhard Manzke, Systemic factors in alveolar bone loss, J Prosthet Dent. 1974;31,5:486-505.  Atwood, DA. Some, clinical factors related to rate of resorption of residual ridges. J Pros Dent 1962; 12:441-50.