This document provides a comprehensive overview of alveolar bone, including its anatomy, classification, composition, histology, and functions. It details bone formation processes, types of bone, the role of different cells involved in bone metabolism, and the clinical implications of alveolar bone health. The document highlights the importance of alveolar bone in supporting teeth and its dynamic nature in response to dental and physiological changes.

1. ALVEOLAR BONE
-HARIPRIYA RAJARAM
DEPT OF PERIODONTICS
PANINEEYA DENTAL COLLEGE
HYDERABAD

2. CONTENTS
• Introduction;
• Functions
• Classification;
• Composition;
• Alveolar bone
• Histology;
• Bone formation;
• Bone resorption;
• Bone remodelling;
• Vascular supply;
• Lymphatic
drainage
• Nerve supply;
• Clinical
application.

3. INTRODUCTION
• Bone is a specialized, rigid,
mineralized connective tissue.
• It is one of the hardest
structures of the animal body.
• Highly vascular.
• Forms the body skeleton
• The human skeleton is the
internal framework of the
body. It is composed of 270
bones at birth – this total
decreases to 206 bones by
adulthood after some bones
have fused together.

4. FUNCTIONS
• It provides shape and support to the body.
• Protects the vital organs of the body.
• Gives attachment to muscles and tendons,which are essential
for locomotion.
• Acts as a storage site for minerals such as calcium and
phosphate.
• It provides the medium, the marrow for the development and
storage of blood cells.
• It possesses a certain degree of toughness and elasticity to the
body.

5. CLASSIFICATION OF
BONE
Based on
shape
Long
Short
Flat
Irregular
Based on
development
Intramembrano
us
Endochondral
Based on
microscopic
structure
MATURE
Compact
Cancellous
IMMATURE OR
WOVEN BONE

6. LONG BONES:
Longer than they are wider.
They have a tubular diaphysis
or shaft,made up of compact
bone surrounding the central
marrow cavity which contains
yellow marrow.
The two bulky ends are called
epiphysis. They are made up of
compact bone at the periphery
and central spongy bone.

7. Epiphyseal line is present
between the epiphysis and
diaphysis.
This is a remnant of
epiphyseal plate.
Eg:arm:humerus,radius,ulna
leg: femur, tibia, fibula,
fingers and toes-each
phalanx
metacarpals and
metatarsals

8. SHORT BONES
These bones are usually cube
shaped of nearly equal length
and width.
They consist of spongy bone
with a thin layer of compact
bone.
Eg; bones of wrist and ankle.

9. FLAT BONES
Flat, thin, curved with no
marrow cavity.
Spongy bone is present
between upper and lower
layer of compact bone.
Eg;sternum,ribs,scapula,cla
vicle and bones that form
roof of skull.

10. IRREGULAR BONES
 Complex shapes
 Notched or with ridges
 Spongy bone covered with
thin layer of compact bone
Eg; bones of
vertebrae,ethmoid.sphenoid,
pelvic bones,calcareous and
mandible.

11. SEASAMOID BONES
Develop in tendons where is
considerable
pressure,tension or friction.
Eg patella

12. IMMATURE OR WOVEN
BONE
MATURE OR LAMELLAR BONE
Intertwined collagen fibers, oriented in
many directions.
Orderly arrangement of collagen. Fibers
in one lamella are at right angles to
collagen in other lamella
Great amount of interfibrillar space less amount of interfibrillar space.
in H&E sections ,the matrix appears
blue due to higher proteoglycan content
Comparatively uniform acidophilic
staining of the matrix.
Faster rate of deposition and
mineralization.
Comparatively slower rate of deposition
and mineralization.
Woven bone is enriched in BAG -75
and bone sialoprotein.
Lamellar bone is enriched in osteocalcin.

13. D
Mineral density is lower Mineral density is higher
Higher water content Lesser water content.
Can entirely be removed by osteoclasts Only a portion of lamellar matrix is
resorbed at once.

14. COMPOSITI
ON
ORGANIC
TYPE 1
COLLAGEN(95%
)
TYPE 5 (5%)
NON COLLAGENOUS
PROTEINS
Osteocalcin
Osteopontin
Osteonectin
Bone sialoprotein
proteoglycans
INORGANIC
calcium, phosphate,
hydroxyl ,
Carbonate ,citrate
and trace amount
of other ions.
The mineral salts
are in the form of
Hydroxyapatite
crystals.

15. OSTOCALCIN First non collagenous protein to be
recognised.
Also known as bone Gla protein as it
contains γ-carboxy glutamic acid.
Secreted by osteoblasts.
Acts as a marker of new bone formation as it
is secreted by osteoblasts.
The carboxy terminal of it is a
chemoattractant to osteoclast precursors
suggesting its role is bone resorption.
OSTEOPONTIN AND
BONE SIALOPROTEIN
Though they have similar structure,they differ in
their functions.Bone sialoprotein is involved in the
initiation of mineral crystal formation.
Osteopontin is a potent inhibitor of hydroxyapatite
crystal growth.
OSTEONECTIN It is a secreted calcium binding glycoprotein.
Plays a role in regulation of cell adhesion,
proliferation, and modulation of cytokine activity.
PROTEOGLYCANS Regulate fibrillogenesis

16. ALVEOLAR BONE
• It is defined as the part of the maxilla and the mandible that
forms and supports the tooth socket.
• It forms when tooth erupts to provide the osseous attchment to
the forming PDL, it disappears gradually after the tooth is lost.
• They are the tooth dependant bony structures as they develop
and undergo remodelling with tooth formation and eruption.
• The size, shape , location and function of the teeth determine
the morphology of the alveolar bone.

17. FUNCTIONS
• Houses the roots of teeth
• Anchors roots of teeth to alveoli with the help of sharpey’s
fibers.
• Helps to move the teeth for better occlusion.
• Helps to absorb and distribute occlusal forces
• Supplies vessels to Periodontal ligament
• Houses and protects developing permanent teeth , while
supporting primary teeth.
• Organizes eruption of teeth

18. STRUCTURE OF ALVEOLAR PROCESS
• Alveolar process has two parts alveolar bone proper and the
supporting alveolar bone
1.Alveolar bone proper consists partly of lamellated and partly
of bundle bone.
• Bundle bone: Is that bone in which principal fibers of pdl are
anchored. Radiographically, it is also referred to as lamina
dura, because of increased radiopacity,which is due to
presence of thick bone without trabeculations.
• Alveolar bone proper which forms the inner wall of the socket
is perforated by many openings that carry branches of the
interalveolar nerves and vessels into the periodontal ligament,
and it is therefore called the cribriform plate.

20. 2. Supporting alveolar bone consists of two parts: cortical
plates and spongy bone
• Cortical plates consist of compact bone and form the outer and
inner plates of alveolar processes.
• They are much thinner in maxilla than in mandible
• They are thickest in the premolar and molar region of the
lower jaw, especially on the buccal side.
• Spongy bone fills the area between the cortical plates and
alveolar bone proper.

21. • In the region of the anterior teeth of both jaws , the
supporting bone is very thin. No spongy is found here.

22. • Cortical bone and alveolar bone proper meet at the
alveolar crest usually 0.75-1.49mm below the
cementoenamel junction on the tooth it surrounds.

23. HISTOLOGY OF BONE

24. • Osteoid is an
unmineralized bone matrix
on the surface, where active
bone formation is taking
place.
• All mature bones have
outer sheet of dense
compact bone and central
medullary cavity. The cavity
shows network of
trabeculae.
• Outer aspect of compact
bone consists of dense
fibrocollagen layer the
periosteum.

25. • Periosteum has two layers:
outer fibrous layer and inner
osteogenic layer
• The inner surfaces of
compact and cancellous
bones are covered by a thin
cellular layer called
endosteum.

26. • CIRCUMFERENTIAL LAMELLAE: They are present at
the periosteal and endosteal surface arranged parallelly.
• HAVERSIAN SYSTEM / OSTEON : Deep to the
circumferential lamellae ,the concentric lamellae are arranged
concentrically around HAVERSIAN CANAL together
known as the haversian system.
• The adult bones, in between the osteons contain interstitial
lamellae.
• Adjacent haversian canals are interconnected by
Volkmann’s canals.

27. • REVERSAL LINES/
CEMENTING LINES
A cement line of
mineralized matrix
delineates the haversian
system. It marks the limit of
bone erosion prior to the
formation of osteon and is
therefore also known as
reversal line. It is highly
irregular.
• RESTING LINES:
This lines has more
regular appearance which
denotes period of rest
during bone formation.

28. • 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 cells in bone tissue.
1. OSTEOPROGENITOR cells
2. OSTEOBLASTS
3. OSTEOCYTES
4. OSTEOCLASTS

29. 1. OSTEOPROGENITOR CELLS
• The osteoprogenitor cells are divided into two types
determined and inducible.
• The DOPC are present in the bone marrow,endosteum,and
periosteum and differentiate into osteoblasts under the
influence of systemic and bone derived growth factors.
• The IOPC represent mesenchymal cells present in other organs
and tissues and differentiate into bone forming cells when
stimulated.
• They express transcription factors which are essential for
osteoblast differentiation.

30. .
2.OSTEOBLASTS
• Osteoblasts are mononucleated cells
responsible for the synthesis and secretion
organic constituents of bone matrix,
remodelling and bone mineralization.
• These are derived from osteoprogenitor cells
of mesenchymal origin.
• Osteoblasts exhibit high level of alkaline
phosphatase which have been recognized as
a reliable indicator of osteoblastic activity.
• The osteoblasts recognize resorptive signal
and transmit it to the osteoclast.

31. REGULATION OF OSTEOBLAST ACTIVITY
PARTHORMONE REGULATES SERUM CALCIUM LEVEL BY
STIMULATION OF BONE RESORPTION
VITAMIN D3 ENHANCES BONE FORMATION -LOW CONCENTRATION
AND RESORPTION -HIGH CONCENTRATION
GROWTH HORMONE REQUIRED FOR ATTAINING NORMAL BONE MASS.
INSULIN STIMULATES BONE MATRIX FORMATION AND
MINERALIZATION
BONE
MORPHOGENIC
PROTEIN
BMPs 2,4,6 DIRECT PLURIPOTENT CELLS TO COMMIT
TO AN OSTEOBLAST LINEAGE.
ALSO INCREASE DIFFERENTIATION OF COMMITTED
CELLS TO OSTEOBLAST LINEAGE.
INSULIN LIKE
GROWTH FACTOR
INCREASES PROLIFERATION AND PLAY A MAJOR
ROLE IN STIMULATING MATURE OSTEOBLAST
FUNCTION.

32. FIBROBLAST
GROWTH
FACTOR
EXERT EFFECT ON BONE
FORMATION,PRIMARILY THROUGH
INCREASED PROLIFERATION OF
OSTEOPROGENITOR CELLS AND PROMTION
OF OSTEOGENIC DIFFERENTIATION.
GLUCOCORTICOID
S
PROMOTE DIFFERENTIATION OF OSTEOBLSATS
AND STIMULATE BONE MATRIX FORMATION.
PROLONGED TREATMENT WITH IT RESULTS IN
BONE LOSS.
PLATELET
DERIVED
GROWTH FACTOR
PROMOTES OSTEOGENESIS.
BUT MAY ALSO HAVE EFFECT ON BONE
RESORPTION BY THE UPREGULATION OF
COLLAGENASE TRANSCRIPTION AND INCREASE IN
IL-6 EXPRESSION IN OSTEOBLASTS.
VASCULAR
ENDOTHELIAL
GROWTH FACTOR
ACTS DIRECTLY ON OSTEOBLATS TO PROMOTE
OSTEOBLSAT MIGRATION,PROLIFERATION AND
DIFFERENTIATION.

33. 3.OSTEOCYTES
• As the osteoblasts form the bone
matrix, they get entrapped within the
matrix they secrete. They are known
as osteocytes.
• Within the bone matrix , the
osteocyte reduces in size, creating a
space around it, called osteocytic
lacuna.
• Narrow extensions of these lacunae
form channels called canaliculi.
• Osteocytic processes are present
within these canaliculi.
• The main function of these canaliculi
is to bring oxygen and nutrients to
the osteocytes through the blood
vessels and to remove the metabolic
waste products

34. 4. OSTEOCLAST
• Multinucleated giant cells
• Removes bone tissue by removing
mineralized matrix of bone.
• They are large cells approximately
40-100 μm diameter with 15-20
closely packed nuclei.
• The presence of acid phosphatase
distinguishes the osteoclast from
other multinucleated giant cells.
• FORMATION: They are derived
from hemopoietic cells of monocyte
macrophage lineage.

35. REGULATION OF OSTEOCLAST ACIVITY
ESTROGEN SUPPRESSES PRODUCTION OF BONE
RESORBING CYTOKINES INCLUDING IL-1
AND IL-6
VITAMIN D3 AND
PARATHYROID
HORMONE
PROMOTES DIFFERENTIATION OF OSTEOCLASTS
FROM MONOCYTE MACROPHAGE STEM CELL
PRECURSORS
CALCITONIN INHIBITOR OF OSTEOCLAST ACTIVITY.
IL-1,IL-6.IL-8,IL-11 ENHANCE OSTEOCLASTOGENESIS
IL-4,IL-10,IL-12,IL-13,IL-
18
LIMIT OSTEOCLAST FORMATION.

36. TNF-ά STIMULATES DIFFERENTIATION OF
OSTEOCLAST PROGENITORS INTO
OSTEOCLASTS.
OSTEOCLAST
INHIBITORY
LECTIN(OCIL)
INHIBITS OSTEOCLAST FORMATION
TGF-β AND
INTERFERON -γ
INHIBIT PROLIFERATION AND DIFFERENTIATION OF
COMMITTED PRECURSORS INTO MATURE
OSTEOCLASTS
BISPHOSPHONATES SUPPRESS BONE RESORPTION BY CAUSING
OSTEOCLAST APOPTOSIS.
PROSTAGLANDINS POWERFUL MEDIATOR OF BONE RESORPTION AND
ALSO STIMULATES BONE FORMATION.

37. HAEMOPOIETIC TISSUE IN BONE
In newborn infants, the
medullary cavity and all
areas of spongy bone
contain red bone marrow.
In adults , red marrow is
found only in
ribs,sternum,vertebrae,
skull and humerus.
Red marrow contains stem
cells of both
fibroblast/mesenchymal
type and blood cell lineage.
Yellow marrow:
Yellow marrow is seen in
epiphysis of long bones.
In old bones, the marrow is
yellow , with loss of hemopoietic
potential and increased
accumulation of fat cells.
Yellow marrow of the medullary
cavity can revert to red marrow ,
if a person is anemic and needs
increased red blood cell
production.
•,

38. BONE FORMATION:
• The process by which bone forms is called OSSIFICATION.
• Ossification begins around the 6th or 7th week of embryonic
life and continues throughout adulthood
• Bone formation follows one of 2 patterns;
• Intramembranous ossification- refers to the formation of bone
directly on or within the fibrous connective tissue membranes.
• Endochondral ossification- refers to the formation of bone in
hyaline cartilage

39. • Maxilla forms by intramembranous ossification.
• Mandible forms partly by intramembranous and partly by
intra-cartilaginous ossification. Greater part of body, ramus,
condyloid and coronoid process are intra-membranous in
origin. Only the tip of condyloid and coronoid process are of
endochondral origin.

41. • At te site of bone formation:loose mesenchyme
capillaries enter the mesenchyme
center cells differentiate
into osteoblasts
▫
▫ lay down bone matrix

42. • The first small mass of newly formed bone matrix is
an irregular shaped spicule
these spicules gradually lengthen to form
anastomosing structures called trabecullae
this early bone is termed as woven bone.
The new bone formation occurs on the pre existing
bone.This is known as appositional growth

43. • As layers of bone build up by apposition,the
trabecullae thicken and soft tissue space gets
narrowed .This process converts cancellous bone to
compact bone..
• The mechanism of intramembranous bone formation
involves bone morphogenic protein.
BMP
Activates
transcription factor called cbfa1
• Mesenchymal cells osteoblasts

44. ENDOCHONDRAL BONE FORMATION
1.FORMATION OF CARTILAGE
MODEL.
2.GROWTH OF CARTILAGE
MODEL.
3.FORMATION OF BONE
COLLAR.
4.FORMATION OF
PERIOSTEAL BUD.
5.FORMATION OF PRIMARY
OSSIFICATION CENTER.
6.FORMATION OF
MEDULLARY CAVITY.
7.FORMATION OF
SECONDARY OSSIFICATION
CENTER.

45. BONE RESORPTION
• Removal of the mineral and organic components of
extracellular matrix of bone under the action of osteolytic cells
especially osteoclasts .
Sequence of bone resorption:
• 1st phase :
Formation of osteoclast progenitors in hematopoietic tissues.
• Their vascular dissemination.
• Generation of resting preosteoclasts and osteoclast in bone.

46. • 2nd phase
Activation of osteoclasts at the surface of bone.
• 3rd phase
Activated osteoclasts resorbing bone.

47. Alterations in osteoclasts
Osteoclasts undergo changes just
before resorption :
1. Development of ruffled border
Many infoldings of cell membrane
resulting in fingerlike projections of
the cytoplasm creating an extensive
surface suited for resorption.
2. Sealing zone of the plasma
membrane
At the periphery of the ruffled border
plasma membrane is smooth and
closely apposed to bone surface.

48. • Cytoplasm contains contractile actin microfilaments
surrounded by 2 vinculin rings .
• This region is called sealing zone or clear zone.
• Facilitates attachment of osteoclast to resorption sites.
• Creates an isolated microenvironment for resorption.
• Osteoclasts binds to bone by Integrin and
Vitronectin.

49. Removal of hydroxyapatite
The initial phase involves
the dissolution of mineral
component.
Protons are released across
the ruffled border into
resorption zone by proton
pump.
This leads to fall in pH to
2.5-3 in the osteoclast
resorption space leading to
resorption of mineral
content.

50. Degradation of organic matrix
• After dissolution of minerals, organic matrix is is resorbed.
• Proteolytic enzymes suck as cathepsin-K and MMP( 9 &13)
are involved in this process.
• Cathepsin-K degrades major amount of type 1 collagen and
non collagenous proteins.
• MMP is required for osteoclast migration ,bone resorption and
osteoclast differentiation.

51. Removal of degradation products from
lacunae.
• Once liberated from bone, the organic and inorganic particles of
bone matrix are taken in by osteoclast through the ruffled
border.
• They are packed into vesicles.
• These vesicles are then releassed by exocytosis.
• This indicates that the matrix components are released away
from the bone.

52. TRAP- Tartrate resistant acid
phosphatase
• Active enzyme which plays an important role in bone
resorption both inside and outside osteoclast cell.

53. • TENCATE DESCRIBED THE SEQUENCE OF EVENTS
IN THE RESORPTIVE PROCESS:
Attachment of osteoclasts to the
mineralized surface of bone.
creation of sealed acidic environment
through the action of proton pump
which demineralizes bone and exposes
the organic matrix
Degradation of the exposed organic
matrix to its constituent amino
acids via the action of released
enzymes.
Sequestering of mineral ions
and amino acids within the
osteoclast.

54. BONE REMODELLING
Sequence
1.Activation phase :
Stimuli such as-
• Micro-fracture,
• Alteration of mechanical loading
• Insulin growth factor-I (IGFI)
• Tumor necrosis factor-α (TNF-α)
• Parathyroid hormone (PTH)
• Interleukin-6 (IL-6) activate lining cells
• RANKL/ RANK interaction triggers pre-osteoclasts fusion
and differentiation toward multinucleated osteoclasts

55. 2.Resorption phase :
 Once differentiated, osteoclasts adhere to the bone surface
and begin to dissolve bone.
 They resorb the haversian lamellae and a part of the
circumferential lamellae and form a resorption tunnel or
cutting cone.
3. Reversal phase :
• After removal of debris produced during matrix degradation,
osteoclasts are replaced by osteoblasts

56. 4.Formation phase:
• Bone matrix resorption leads to the release of several growth
factors:
• Bone morphogenetic proteins (BMPs)
• Fibroblast growth factors (FGFs)
• Transforming growth factor β (TGF β)
• Recruitment of the osteoblasts in the reabsorbed area
• Osteoblasts produce the new bone matrix

58. MEDIATORS OF BONE REMODELING
HORMONES
• Parathyroid hormone
• Vitamin D metabolites
• Estrogen
• Growth hormone
• Glucocorticoids

59. LOCAL FACTORS
• IL-1
• TNF- α and TNF- β
• Prostaglandins
• IGF-1 and II
• Bone morphogenic protein
• Bacterial products
 MECHANICAL FACTOR
• Under muscular action, tension is transmitted to the
bone ,which is detected by osteocyte network. These
osteocytes produce prostaglandins and IGF-1 which
stimulate osteoblast activity leading to increased
bone formation.

60. MARKERS OF BONE FORMATION
• Alkaline phosphatase
• Osteocalcin
• Procollagen 1 extension peptide
MARKERS OF BONE RESORPTION
• Urine calcium
• Urine hydroxyproline
• Collagen crosslink fragments
• Urine N-telopeptide
• Urine C-telopeptide
• Urine total pyridinoline
• Urine free deoxypyridinoline

61. VASCULAR SUPPLY

62. LYMPHATIC DRAINAGE

63. NERVE SUPPLY

64. ALVEOLAR BONE IN DISEASE

65. Conditions involving loss of alveolar bone
■ The various causes of alveolar bone loss are:
I. Extension of gingival inflammation
II. Trauma from occlusion
III. Systemic factors
Other factors :
I. Periodontitis
II. Periodontal abscess
III. Food impaction
IV. Overhanging restoration
V. Adjacent tooth extraction
VI. Ill-fitting prosthesis

66. BONE DESTRUCTION CAUSED BY
EXTENTION OF GINGIVAL INFLAMMATION
• Most common cause of bone loss in periodontal disease is
extension of inflammation from marginal gingiva into
supporting periodontal tissues.
• The transition from gingivitis to periodontitis is associated
with changes in compostion of bacterial plaque.
• In advanced stages number of motile organisms and
spirochetes increases.
• The cellular composition of the infiltrated connective tissue
also changes with increasing severity of the lesion

67. Radius of action of plaque
■ Garant &Cho suggest that bacterial plaque can induce
bone loss within range of 1.5 to 2.5 mm.
■ Page and Schroeder on the basis of waerhaug’s
measurements made on human autopsy specimens,
postulated that there is range of effectiveness of about
1.5 to 2.5mm within which bacterial plaque can induce
loss of bone. This is known as radius of action.

68. BONE DESTRUCTION PATTERN IN
PERIODONTAL DISEASE
1)Horizontal bone loss
2)Vertical bone loss
Horizontal bone loss:
■ Most common pattern of bone
loss in periodontal disease.
■ Bone is reduced in height but
margin remains approximately
perpendicular to tooth surface.

69. VERTICAL BONE LOSS
 Vertical/angular bone loss
occurs in an oblique
direction.
 The base of the defect is
apical to the surrounding
bone.
 It occurs when the pathway
of inflammation travels
directly into the pdl space.
 This type of bone loss
produce infrabony pocket.

70. • Goldman and Cohen classified angular defects on
the bases of number of osseous walls.
•
•
• three walled
•
• two walled
• one
• walled combined defect

71. • REVERSAL OF ARCHITECTURE:
Produced by loss of interdental bone, including
facial and lingual plates without concomitant
loss of radicular bone, there by reversing the
architecture.

72. CRATERS
• These are specific type of two-walled defects;the
present as concavities in the crest of interdental
bone that is confined within the facial and
lingual walls.

73. BULBOUS BONE CONTOURS.

74. LEDGES
• Plateau like bone margins caused by resorption of
thickened bony plates

75. TRAUMA FROM OCCLUSION
 When occlusal forces exceeds the adaptive capacity of the
tissue , tissue injury results Trauma from occlusion
 1) ACUTE TRAUMA FROM OCCLUSION
 2) CHRONIC TRAUMA FROM OCCLUSION
 PRIMARY TRAUMA FROM OCCLUSION:
 Alteration in occlusal forces with normal periodontium with
normal height of bone.
 SECONDARY TRAUMA FROM OCCLUSION:
 Due to reduced ability of tissues to resist forces .

76. FENESTRATION
• Isolated areas in which root is denuded of bone and the root
surface is covered only by periosteum and underlying gingiva
are termed as fenestration. Here the marginal bone is intact.
DEHISCENCE
• When the denuded areas extend through the marginal bone,
the defect is called as dehiscence.

77. Bone Destruction by Systemic
Disease
 Vit-D deficiency
 Diabetes
 Hyperparathyroidism
 Paget’s disease
 Fibrous dysplasia
 Osteoporosis
 Osteopetrosis

78. DISEASES
OSTEOPOROSIS
• Osteoporosis is a common condition characterized by both
alterations in the macro and micro architecture of the bone.
• There are multiple etiologies of this systemic disease,including
post menopausal,age associated, glucocorticoid induced,
secondary to cancer, androgen ablation, and aromatase
inhibitors (Kanis 2002).
• All these forms result in decrease in strength and cause
fractures.
• Post menopausal osteoporosis is the most common cause.
• There is a decrease in bone mineral density.

79. OSTEOPETROSIS
Osteopetrosis is a group of related diseases in which there is a
pronounced increase in BMD due to abnormal bone turnover.
They are due to a variety of defects in osteoclastic bone
resorption.

80. VITAMIN D DEFICIENCY
When inadequate vitamin D is available, mineralization of the bones
is impaired, resulting in a condition referred to as osteomalacia.
When the disease occurs in children, it is referred to as rickets.
The key features of osteomalacia are bones that contain a normal
collagen matrix and osteoid structure, but lack proper
mineralization, resulting in the softening of bones(Russell2010).

81. DIABETES MELLITUS
• Chronic hyperglycemia adversely affects the synthesis,
maturation and maintenance of collagen and extracellular
matrix.
• Hyperglycemia results in formation of accumulated glycation
end products .
• Collagen is crosslinked with AGE formation , which makes
the collagen less soluble and less likely to be normally
repaired or replaced resulting in bone loss

82. OSTEONECROSIS
When ischemia occurs in bone for an extended
period of time, often due to an interruption in blood supply,
cell death occurs.
Osteonecrosis has multiple etiologies including radiation,
bisphosphonate use, steroid use, hypertension, and in some
cases arthritis or lupus.
Bisphosphonate‐related osteonecrosis of the jaw (ONJ) is of
growing concern in the dental field.

83. HYPERPARATHYROIDISM
 Hyperparathyroidism is an overproduction of PTH, which
promotes resorption of calcium and phosphorus from bone
to increase serum calcium to normal levels (Unnanuntana et
al. 2011)
 Primary hyperparathyroidism is most commonly caused by
a parathyroid gland adenoma, whereas secondary
hyperparathyroidism occurs when PTH production is
overstimulated in response to low serum calcium.
Tooth mobility, malocclusion, osteoporosis, widening of pdl
space and loss of lamina dura are the oral manifestations.

84. PAGETS DISEASE
• Paget’s disease is a condition where bone metabolism is
significantly higher than normal, with bone formation
exceeding that of resorption (Noor & Shoback2000). This
results in excessive bone formation and may affect one or
multiple bones.
• The affected bones, despite having increased bone formation,
are weak and deformed.
• This is due to irregular collagen fiber formation within the
bones.

85. FIBROUS DYSPLASIA
• Fibrous dysplasia is a skeletal developmental anomaly
of the bone-forming mesenchyme that manifests as a
defect in osteoblastic differentiation and maturation
• Symptoms of this condition include fractures and bone pain.
• Notably, this condition has other craniofacial symptoms,
including craniofacial bone deformities, exophthalmos, and
dental abnormalities.

86. THERAPEUTIC CONSIDERATIONS.
• Tumour necrosis factor-α antagonists.
• Inhibitors of cytokines.
• Inhibitors of RANK/RANKL
• Hormone replacement therapy
• Cathepsin inhibitors.
• Bisphosphonates.
• NSAIDS
• Statins.
• GRAFTS

87. CONCLUSION
• It is a rigid ,specialized connective tissue.
• Its formation and function is dependant on the
dentition.
• It is of utmost importance for the healthy
periodontium.

88. REFERENCES:
• Carranza’s Clinical Periodontology, 13th edition.
• Clinical Periodontology & Implant Dentistry, 6th
edition, Jan Lindhe
• Orban’s oral histology and embryology 13th th
edition
• Marie PJ Bone remodeling: a social network of
cells . Medicographia. 2012;34:149-154
• Bartold, P. M., Cantley, M. D., & Haynes, D. R.
(2010). Mechanisms and control of pathologic
bone loss in periodontitis. Periodontology 2000,
53(1), 55–69