This document provides an overview of bone physiology. It begins with definitions of bone and its functions, including supporting the body, protecting organs, and allowing movement. It then covers the classification, anatomy, histology, composition, growth and remodeling of bone. Key points include that bone is made up of inorganic minerals and organic collagen matrix, and is in a constant state of breakdown and formation through the actions of osteoclasts and osteoblasts, maintaining homeostasis. The document provides details on intramembranous and endochondral ossification, as well as the structure of alveolar bone and its importance for dentistry.

1. PRESENTEDBY –
Dr.Pushkardwivedi
PG 2ND
YEAR
DEPT. OF PROSTHODONTICS
BONE PHYSIOLOGY

2. CONTENTS
Introduction-
Definition
Function of bone
Classification of bone
Anatomy of bone
Types of bone
Composition
Structure of alveolar process
Ossification process
Functional zone

3. 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

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. Periodontists tries to maintain the
maximum amount of alveolar support around the roots of the teeth.

5. 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

8. CLASSIFICATION OF BONES: BY POSITION

9. 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

10. 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)

11. 3) FLAT BONES-
•Thin, flattened and a bit curved
(e.g sternum & most skull bones)

12. 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

13. CLASSIFICATION OF BONES:
BY GROSS STRUCTURE
Compact boneCompact bone
Spongy boneSpongy bone
BY DEVELOPMENT
Membranous ( ectodermal) boneMembranous ( ectodermal) bone
Cartilaginous ( endochondral ) boneCartilaginous ( endochondral ) bone

14. ANATOMY: STRUCTURE OF BONE
A typical long bone consist of following
Diaphysis
Epiphysis
Metaphysis
Articular cartilage
Periosteum
Medullary or marrow cavity
Endosteum

15. 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

16. 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.

18.  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.

19.  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.

20.  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.

21. 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

22. 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.

23. 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

24. 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.

25. Interstitial lamellae
Concentric lamellae

26. 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.

27. 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

28. 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.

29. 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.

30. 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)

31. 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)

32. 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.

33. 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.

34. 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

35. 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.

40. 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

41. 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)

42. 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.

43. 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)

44. 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.

45. •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.

46. 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

47. 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..

48. 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)

49. 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

50. Long Bone Growth and Remodeling

51. 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

52. 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

53. 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.

54. 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

55. 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

56. Repair of bone after fracture

57. 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

58. 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.

59. 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.

60. 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.

61. 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.

62. 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

63. 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.

64. 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.

65. 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

66. 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)

67. 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.

68. 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

69. 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
.

70. BONE CLASSIFICATION SCHEMES
RELATEDTO IMPLANT DENTISTRY

72. 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-

73. 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.

74. 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

75. 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.

76. 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

77. 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

78. 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

79. 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.

80. 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

81. 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

82. -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

83. References-
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