from basics to pg level

1. ALVEOLAR BONE
by
Dr YAMINI UNNI

2. CONTENTS

5. OVERVIEW OF BONES :
WHAT & WHY WE NEED THEM?
Bone is a dynamic biological tissue,
composed of various metabolically
active cells that are integrated into a
rigid framework
Enable
Mobility
SUPPORT &
PROTECT
ENDOCRINE
REGULATION
STORE
MINERALS

6. The ALVEOLAR process of bone is defined as that part of the maxilla
and the mandible that forms and supports the sockets of the teeth

7. FUNCTIONS

8. 1
2
3
4

9. 5 6 7

10. HOUSES ROOTS OF THE TEETH
ANCHORS ROOTS OF THE TEETH TO THE ALVEOLI –
INSERTION OF SHARPEY’S FIBRE INTO THE ALVEOLAR BONE PROPER
HELPS TO MOVE THE TEETH FOR BETTER OCCLUSION
HELPS TO ABSORB AND DISTRIBUTE OCCLUSAL FORCES GENERATED DURING
TEETH CONTACT
SUPPLIES VESSELS TO PERIODONTAL LIGAMENT
HOUSES AND PROTECTS DEVELOPING PERMANENT TEETH WHILE SUPPORTING
PRIMARY TEETH
ORGANISES ERUPTION OF PRIMARY AND PERMANENT TEETH

11. GROSS BONE MORPHOLOGY
• DENSE OUTER SHEET-
COMPACT BONE
• CENTRAL-MEDULLARY
CAVITY
CHARACTERISTIC
• IN LIVING BONE
CAVITY FILLED WITH
• RED AND YELLOW
BONE MARROW
FILLING
• EXTREMITIES OF LONG
BONES
• NETWORK OF BONY
TRABECULAE
INTERRUPTION

13. HISTOLOGICALLY IDENTICAL
MICROSCOPIC LAYERS/LAMELLAE
TRABECULAR
COMPACT
MATURE

14. CIRCUMFERENTIAL
CONCENTRIC
INTERSTITIAL
• ENCLOSE ENTIRE ADULT BONE
• FORMS INNER AND OUTER PERIMETER
• BULK OF COMPACT BONE
• FORM BASIC METABOLIC UNIT OF BONE-
OSTEON [HAVERSIAN SYSTEM]
• INTERSPERSED BETWEEN ADJACENT CONCENTRIC
LAMELLAE
• FILL SPACES BETWEEN THEM
• THEY ARE FRAGMENTS OF PREEXISTING CONCENTRIC
LAMELLAE
• FORMED FROM OSTEONS- REMODELLING

16. CONCENTRIC LAMELLAE
CYLINDER OF BONE
ORIENTED
PARALLEL TO THE
LONG AXIS OF THE
BONE
OSTEON
-CANAL LOCATED IN
CENTER OF EACH
BONE
-EACH CANAL HAS
CAPILLARIES
-LINED BY SINGLE
LAYER OF BONE CELLS
THAT COVER THE
BONE SURFACE
HAVERSIAN
CANAL
-INTERCONNECTION
OF HAVERSIAN CANAL
-HAVERSIAN CANAL
HAS THIS VASCULAR
CONNECTIONS
VOLKMANN
CANAL

18. CONNECTIVE TISSUE OF BONE
CONTENTS
TWO LAYERS
MEMBRANE COVERING
OUTER ASPECT OF BONE
PERIOSTEUM
OUTER
LAYER
FIBROUS
LAYER
DENSE
IRREGULAR
CONNECTIVE
INNER
LAYER/
CAMBIUM
LAYER
BONE CELLS-
PRECURSORS-
RICH BLOOD
RICH
MICROVASCULAR
SUPPLY

20. ENDOSTEUM
COVERS INTERNAL SURFACE OF COMPACT AND CANCELLOUS BONE
LOOSE CONNECTIVE TISSUE
OSTEOGENIC CELLS SEPERATES BONE AND MARROW WITHIN

22. HEMATOPOIETIC TISSUE IN BONE
• YOUNG BONE
• FOUND IN CAVITIES OF LONG BONE AND DIPLOE OF FLAT BONES
• STEM CELLS OF BOTH FIBROBLAST/MESENCHYMAL TYPE AND BLOOD CELL
RED
MARROW
• OLD BONE
• SEEN IN EPIPHYSIS OF LONG LONE
• LOSS OF HEMOPOETIC POTENTIAL
• INCREASED ACCUMULATION OF FAT CELLS- YELLOW
• YELLOW REVERT TO RED: ANEMIC AND NEEDS INCREASED RED CELL
PRODUCTION
YELLOW
MARROW

24. COMPOSITION OF BONE

25. CONSTITUENTS OF ALVEOLAR BONE

26. ORGANIC MATRIX

27. CELL ADHESION PROTEINS
OSTEOCLAST
OSTEOBLAST

28. PARACRINE FACTORS
CYTOKINES
CHEMOKINE
LOCAL CONTROL OF
MESENCHYMAL
CONDENSATION
THAT OCCUR ON THE
ONSET OF
ORGANOGENESIS
GROWTH
FACTORS

29. COLLAGEN

31. COLLAGEN
• FORMS HETEROTYPIC FIBER BUNDLES- PROVIDES BASIC
STRUCTURAL INTEGRITY OF CONNECTIVE TISSUE
• ELASTICITY OF COLLAGEN IMPARTS RESILIENCY TO TISSUE
AND RESIST FRACTURE
MAJOR ORGANIC
COMPONENT-
TYPE I COLLAGEN 95%
TYPE V COLLAGEN <5%
• SHARPEY’S FIBRE- TYPE III & TYPE I
• TYPE XII- UNDER MECHANICAL STRAIN
• TYPE III AND XII PRODUCED BY FIBROBLAST DURING PDL
FORMATION
• TYPE I , V , XII – BY OSTEOBLAST
ALVEOLAR BONE –
TYPE I , TYPE V,
TYPE III AND TYPE XII

33. NON COLLAGENOUS PROTEINS
10 %
ORGANIC
CONTENT
ENDOGENOUS
PROTEINS
ALBUMI

34. OSTEOCALCIN
FIRST NON
COLLAGENOUS
PROTEIN
KNOWN AS
Bone Gla protein
CONTAINS
AMINO ACID
PRODUCED BY
OSTEOBLAST
&ODONTOBLAST
¥-CARBOXY
GLUTAMIC ACID
SEEN IN ALVEOLAR
BONE

35. Matrix gla
protein
Mineral
binding
Extracellular
Matrix
Mineralized
vascular
smooth
cells
CHONDROCYTES
ᾰ2hs
glycoprotein-
liver
Inhibition of
apatite
formation by
serum

36. OSTEONECTIN (SPARC)

37. OSTEOPONTIN &
BONE SIALOPROTEIN
OLD NAME- BONE SIALOPROTEIN II
HEAVILY GLYCOSYLATED &
PHOSPHORYLATED
HIGH LEVELS OF ACIDIC AMINO ACIDS

38. OSTEOPONTIN
GENERALIZED
DISTRIBUTION
INHIBITOR OF
HYDROXYAPATITE
CRYSTAL GROWTH
ENRICHED AT
CELL MATRIX
INTERFACE
MEDIATE ATTACHMENT
OF BONE CELLS
INCLUDING OSTEOCLAST
TRANSCRIPTION
STRONGLY
REGULATED BY
VIT D3
EXPRESSION
STIMULATED BY TGF-β
AND
GLUCOCORTICOIDS
RGD PROTEINS
ATTACHMENT OF CELLS TO
BONE MATRIX

39. BONE
SIALOPROTEIN
MINERALIZING
TISSUES
INITIALTION OF
MINERAL CRYSTAL
FORMATION
INVIVO
EXPRESSION
STIMULATED BY TGFβ
GLUCOCORTICOIDS
GLUTAMIC ACID
PREDOMINANT

40. PROTEOGLYCANS
LARGE
• CHONDROITIN SULFATE PROTEOGLYCAN
• NON MINERALIZED BONE MATRIX
SMALL
• BIGLYCAN(CHONDROITIN SULPHATE PROTEOGLYCAN I)
• DECORIN(CHONDROITIN SULPHATE PROTEOGLYCAN II)
• THIRD SMALL PROTEOGLYCAN FOUND IN MINERAL CRYSTALS

41. BIGLYCAN
• PROMINENT IN DEVELOPING BONE AND MINERAIZES TO PERICELLULAR AREA
• IT CAN BIND TO TGF-β AND EXTRA CELLULAR MATRIX MACROMOLECULES INCLUDING
COLLAGEN
• REGULATE FIBRILLOGENESIS
DECORIN
• BINDS MAINLY WITHIN THE GAP REGION OF COLLAGEN FIBRILLS AND DECORATES FIBRIL
SURFACE
• PRIMARY CALCIFICATION IN BONES- REMOVAL OF DECORIN AND FUSION OF COLLAGEN
FIBRILS

42. TRAMP AND LYSYL OXIDASE
• TYROSINE RICH ACIDIC MATRIX PROTEINS
• DEMINERALIZED BONE + DENTIN MATRIX
• TGF- β AND DECORIN BINDING
• TOGETHER THESE PROTEINS REGULATE THECELLULAR RESPONSE TO
TGF-β
‘TRAMP’
DERMATOPONTI
• ‘CRITICAL ENZYME’
• COLLAGEN CROSS LINKING
• SAME ACTION OF ‘TRAMP’
• PROCOLLAGEN PEPTIDES,THROMBOSPONDIN,FIBRONECTIN,VITRONECTIN,
ALKALINE PHOSPHATASE – OTHER ENZYMES FOUND IN BONE
LYSYL OXIDASE

44. INORGANIC MATTER
IONS- CALCIUM
PHOSPHATE,
HYDROXYL,CARBONAT
BONE CRYSTALS-
PLATE /LEAF LIKE
STRUCTURE
CARBONATE WITH
LOW Ca /P RATIO
HYDROXYAPATITE
MINERAL
COMPONENT

48. BONE AND BONE LINING CELLS
OSTEOBLAST
OSTEOCYTES
OSTEOCLAST

50. DEVELOPMENT OF BONE CELL

51. OSTEOBLAST
MONONUCLEATED CELLS MACROMOLECULAR ORGANIC CONSTITUENTS OF
BONE MATRIX
{ SYNTHESIS &SECRETION}
DERIVED FROM- OSTEOPROGENITOR CELLS
(MESENCHYMAL ORIGIN)
DURING CHILDHOOD GROWTH AFTER SKELETAL FRACTURES
PERIOSTEUM SERVES AS RESERVOIR
BONE FORMING TUMORS

52. MORPHOLOGY

55. SECRETORY GRANULES
THESE GRANULES RELEASE CONTENTS ALONG THE SURFACE OF CELL- OPPOSED TO FORMING BONE-
ASSEMBLE EXTRACELLULARLY AS FIBRILS TO FORM OSTEOID
GOLGI COMPLEX- PALE JUXTANUCLEAR AREA (SITE)
PROCOLLAGEN + ORGANIC CONSTITUENTS OF BONE ENTER ITS LUMEN
TRANSFERRED AND ASSEMBLED IN GOLGI COMPLEX INSIDE SECRETORY GRANULES
ABUNDANT,WELL DEVELOPED SYNTHETIC ORGANELLES
INTENSE CYTOPLASMIC BASOPHILIA- ↑ ROUGH ENDOPLASMIC RETICULUM

56. ARRANGEMENT
THIS CONNECTION PROVIDES INTERCELLULAR
ADHESION &CELL TO CELL COMMUNICATION
ENSURES THE OSTEOBLAST LAYER COMPLETELY COVERS
OSTEOID SURFACE AND FUNCTIONS IN COORDINATED
CANALICULI FORMATION-
ORGANIC MATRIX DEPOSITED AROUND CELL BODIES AND CYTOPLASMIC PROCESS
CELL CONTACT EACH OTHER BY GAP JUNCTIONS
AND ADHERENS
FUNCTIONALLY CONNECTED TO MICROFILAMENTS AND
ENZYMES THROUGH SECONDARY MESSENGER SYSTEM
NUCLEUS SITUATED ECCENTRICALLY-
AWAY FROM ADJACENT BONE SURFACE
NON COLLAGENOUS PROTEIN
RELEASED AND DIFFUSED ALONG OSTEOBLAST
SURFACE
PARTICIPATE IN REGULATING MINERAL
DEPOSITION

58. OSTEOBLAST FORMATION

59. OSTEOBLAST FORMATION

61. DETERMINED OSTEOGENIC PRECURSOR CELLS (DOPC’S)
PRESENT IN BONE MARROW, ENDOSTEUM,PERIOSTEUM
DIFFERENCIATED WITH HELP OF SYTEMIC AND BONE DERIVED
GROWTH FACTORS
OSTEOBLAST
INDUCIBLE OSTEOGENIC PRECURSOR CELLS (IOPC’S)
REPRESENT MESENCHYMAL CELLS PRESENT IN OTHER
ORGANS/TISSUES
STIMULATED
OSTEOBLAST

62. FUNCTIONS
• NEW BONE FORMATION
• VIA SYNTHESIS OF PROTEINS AND
POLYSACCHARIDES
MAIN
FUNCTION
• REGULATION OF BONE
REMODELLING
• MINERAL METABOLISM
OTHER
FUNCTIONS

63. MINERALIZATION OF OSTEOID
OSTEOBLAST SECRETE TYPE 1
COLLAGEN
WIDELY DISTRIBUTED
SECRETION
TYPE V COLLAGEN OSTEONECTIN
OSTEOPONTIN
RANKL, OSTEOPROTEGERIN
PROTEOGLYCANS GROWTH
FACTOR(BMP)
HORMONES
PTH, VIT D3 ESTROGEN
GLUCOCORTICOIDS
OSTEOBLAST DIFFERENCIATION
RECOGNISE RESORPTIVE SIGNALS –
TRANSMIT TO OSTEOCLAST

66. FOURSCHEMES
OSTEOBLAST ARE UNPOLARIZED, LAY DOWN BONE IN ALL
DIRECTIONS
SAME GENERATION ARE POLARIZED:
OSTEOBLASTS ARE POLARIZED IN THE SAME DIRECTION. ONE GENERATION
BURIES PRECEDING ONE IN BONE MATRIX
WITHIN ONE GENERATION:
SOME OSTEOBLAST SLOW DOWN RATE OF DEPOSITION/STOP LAYING DOWN
BONE
HOW OSTEOBLAST GETS TRAPPED

68. OSTEOBLAST
HAS 4 FATES
EMBEDDED
IN BONE -
OSTEOCYTE
INACTIVE
OSTEOBLAST
-BONE
LINING
UNDERGO
APOPTOSIS
CELLS THAT
DEPOSIT
CHONDROID
AND
CHONDROID
BONE

69. BONE LINING CELLS
REMAIN ON SURFACE-
LINING CELLS
ENTRAPPED IN BONE
MATRIX- OSTEOCYTES
REMOVES MINERALIZED
MATRIX OF BONE
REMOVES BONE TISSUE
“BONE AND BROKEN”
OSTEOCYTES
OSTEOCLAST

71. OSTEOCYTES
• Microscopically osteocytes are lost
• Cavties are filled with debris
Woven and repair bone has
↑ osteocytes than lamellar
bone
• In bone matrix osteocyte reduce in size creating space
around it.
• Narrow extentions of lacunae form channels called
canaliculi.
OSTEOCYTIC LACUNA

73. Old osteocytes retract their process from
canaliculi and when dead the lacunae and
canaliculi get plugged with debris
Death of osteocytes leads to
resorptionof the matrix of osteoclasts
Osteocytes secrete few
matrix protein

74. OSTEOBLAST TO OSTEOCYTE TRANSFORMATION

75. ALVEOLAR BONE
CONTINUED…..

77. MECHANISMS OF TRANSORMATION

78. OSTEOCLAST

80. RANKL
RECEPTOR ACTIVATOR OF NUCLEAR FACTOR Κ B- ligand
Member of the tumor necrosis factor (TNF) cytokine family
It binds to RANK on cells of myeloid lineage
It functions as a key factor for osteoclast differenciation and activation
RANKL may also bind to OPG
RANKL helps in dendritic cell function

81. OSTEOPROTEGRIN- OPG
• Osteoprotegerin (OPG) is secreted by
osteoblasts and osteogenic stromal stem cells
and protects the skeleton from excessive bone
resorption by binding to RANKL and preventing
it from interacting with RANK.

82. FORMATION
CFU-GM (GRANULOCYTE
MACROPHAGE COLONY
FORMING UNIT
COMMITTED PRECURSOR
CELLS
PRE-OSTEOCLASTS(Immature
multinucleated giant cell)
RANK on the surface
Stromal cells/osteoblasts secrete
• RANK-L (ODF-osteoclast
differenciation factor)
• M-CS F(Macrophage colony
stimulating factor)
OPG expressed by osteoblasts
inhibits RANK-RANKL Interaction
INHIBITION OF OSTEOCLAST
DIFFERENCIATION &ACTIVITY
INTERACTION OF
RANK & RANKL
FULLY FUNCTIONAL OSTEOCLAST

83. Regulation of osteoclast formation in cortical (A)
and trabecular (B) bone.
At the periosteal site of cortical bone [(A), left],
ATRA stimulates RANKL production in osteoblasts
and/or osteocytes which leads to stimulation of
differentiation of mature osteoclasts from osteoclast
progenitors.
In bone marrow or at endosteal site [(A), right],
ATRA does not stimulate RANKL formation but
inhibits differentiation of osteoclast progenitors to
mature osteoclasts.
The role of ATRA for osteoclast formation on the
endosteal surfaces of trabecular bone

84. FACTORS FAVOURING FORMATION
TRANSCRIPTION FACTORS
LOCAL AND SYSTEMIC FACTORS
a. Hematopoeitic factors
b. Cytokines
c. Hormones
Vit d3 , pth , PGE2 , GLUCOCORTICOIDS
FACTORS LIMITING FORMATION
DIFFERENCIATION : OPG , OCIL
LOCAL AND SYSTEMIC FACTORS
a. Growth hormones-TGFβ IGF-1 IGF11
b.hormones;glucocorticoids,pth,PGE2,
calcitonin , estrogen
c.cytokines: IL-4,10,12,13,18
d. pharmacological:bis phosphonates
FACTORS REGULATING OSTEOCLAST FORMATION

85. The ruffled border is composed of many tightly
packed microvilli adjacent to the bone surface,
providing a large surface area for the resorptive
process.
Cathepsin containing vescicles and
vacuoles are present closed to ruffled
border indicating resorptive activity of
Rich in acid phosphatase and other lysozyme.
synthesized in RER transported to golgi
and moved to the ruffled border in transport
vesicles , they release their content into the
bone surface.

86. SEALING/CLEAR ZONE
At the periphery of the ruffled border, the
plasma membrane is smooth and closely
apposed to the bone surface.
The adjacent cytoplasm, devoid of cell
organelles contains contractile actin
microfilaments.
This region is called CLEAR/SEALING ZONE.
This zone, thus creates an isolated
microenvironment in which resorption can
take place.

87. Osteoclasts lie in resorption bays called Howship’s
lacunae
Cutting Cone

88. Several osteoclasts excavating
a large area on bone which is the
leading edge of resorption is
termed as the Cutting cone.
Released cytokines (BMP &
IGF) stimulate stem cells to
differentiate into osteoblasts.
THESE OSTEOBLASTS
OSTEOID KNOWN AS FILLING
CONE

89. BONE FORMATION
1. INTRAMEMBRANOUS OSSIFICATION
2. INTRACARTILAGENOUS OSSIFICATION (ENDOCHONDRAL)
3. IMMATURE VS MATURE/WOVEN VS LAMELLAR

95. INTRACARTILAGENOUS / ENDOCHONDRAL BONE FORMATION

103. BONE RESORPTION
• Complex process
• Appearence: Eroded bone surface(Howship’s lacunae) large multinucleated cells(osteoclast)
• Osteoclast:
• origination: hematopoietic tissue.
• formation: fusion of mononuclear cells of asynchronous population.
• Appearance: Ruffled border(elaborately developed)
• Secretion: hydrolytic enzymes(digest organic portion of bone)
• Regulation: activity and morphology regulated by enzymes
(PTH and calcitonin-receptors on osteoclast membrane.)

105. TENCATE’S SEQUENCE
• Attachment of osteoclast to the mineralized surface of bone.
• Creation of a sealed acidic environment through action of the proton pump ,
which demineralises bone and exposes organic matrix.
• Degradation of the exposed organic matrix to its constituent amino acids-by
the action of released enzymes-phosphatase and cathepsin.
• Sequestering of mineral ions and amino acids within the osteoclast.

106. TEN CATE’S SEQUENCE

108. STRUCTURE OF ALVEOLAR BONE

110. EXTERNAL PLATE OF CORTICAL BONE
Haversian bone +compact bone lamellae
ALVEOLAR BONE PROPER/CRIBRIFORM PLATE/LAMINA DURA
CANCELLOUS TRABECULAE/TRABECULAR BONE
INTERDENTAL SEPTA
INTERRADICULAR SEPTA
BASAL BONE

113. ALVEOLAR BONE PROPER
ALVEOLAR BONE PROPER
A THIN LAMELLAE OF BONE THAT SURROUNDS THE ROOTS OF THE TOOTH
AND GIVES ATTACHMENT TO PRINCIPAL FIBERS OF THE PERIODONTAL
LIGAMENT-
LAMELLATED BONE- SOME LAMELLAE OF BONE ARE ARRANGED
PARALLEL TO THE SURFACE OF ADJACENT MARROW SPACES.OTHERS FORM
HAVERSIAN SYSTEM
BUNDLE BONE: THE PRINCIPAL FIBERS OF PERIODONTAL LIGAMENT
ARE ANCHORED INTO THE BONE.

114. ALVEOLAR BONE PROPER
ZUCKERKANDL AND HIRSCHFELD CANALS (nutrient canals)
Nutrient canals are anatomic structures of the alveolar bone through which neurovascular elements transit to supply teeth and
CRIBRIFORM PLATE
A SERIES OF OPENINGS THROUGH WHICH NEUROVASCULAR BUNDLES LINK THE PERIODONTAL LIGAMENT WITH CENTRAL
COMPONENT OF BONE- CANCELLOUS BONE
Alveolar bone proper is a part of alveolar bone that form the inner thin wall of the socket facing the
In radiographs seen as LAMINA DURA HISTOLOGICALLY KNOWN AS CRIBRIFORM PLATE

116. BLOOD SUPPLY-ALVEOLAR BONE PROPER
ALVEOLAR BONE
PROPER
FORMS THE INNER WALL OF
SOCKET
PERFORATED BY BRANCHES
OF INTERALVEOLAR NERVES
AND BLOOD VESSELS
CRIBRIFORM PLATE
BLOOD VESSELS ARE
PERFORATED INTO
PERIODONTAL LIGAMENT
HENCE KNOWN AS CRIBRIFORM
PLATEINTERDENTAL SEPTUM IS THE
BONE BETWEEN TEETH AND
COMPOSED OF CRIBRIFORM
PLATE
NUTRIENT CANALS
INTER DENTAL AND INTER
RADICULAR SEPTA CONTAIN
PERFORATING CANALS-
ZUCKERKANDL AND HIRSCHFELD
THEY HOUSE THE BLOOD
AND LYMPHATIC SUPPLY

117. LAMELLAR BONE
Consist of osteons
• Concentric lamellae with
central blood vessel
CONTINUES WITH
SUPPORTING
ALVEOLAR BONE
• MATURE
BONE
Plywood like
layers
• Arrange
in sheets

118. BUNDLE BONE

120. SUPPORTING ALVEOLAR BONE

123. SPONGY BONE
TYPE II
INTERDENTAL AND INTERRADICULAR TRABECULAE ARE
IRREGULARLY ARRANGED AND DELICATE
LACKS DISTINCT TRAJECTORY PATTERN-SEEN IN MAXILLA
FATTY MARROW SPACES PRESENT
TYPE I
INTERDENTAL AND INTERRADICULAR TRABECULAE ARE
REGULAR AND HORIZONTAL
LADDER LIKE APPEARANCE
SEEN IN MANDIBLE – TRAJECTORY PATTERN
FILLS AREA BETWEEN CORTICAL PLATE AND ALVEOLAR BONE PROPER
TYPE 1 TYPE II

125. ALVEOLAR CREST
SHAPE DEPENDS ON
THE POSITION OF
ADJACENT TEETH
IN HEALTHY- CEJ AND
FREE BORDER OF
ALVEOLAR BONE
PROPER IS CONSTANT
NEIGHBOURING
TEETH INCLINED-
ALVEOLAR CREST IS
OBLIQUE
CORTICALAND
ALVEOLAR BONE
MEET AT ALVEOLR
CREST AT 1.5 -2MM
BELOW LEVEL OF CEJ

127. SOCKET WALL
• DENSE
• LAMELLATED BONE
• BUNDLE BONE
• Bone adjacent to the periodontal ligament
• Large number of sharpey’s fibres.
• Thin lamellae arranged in layers parallel to the
root,with intervening appositional lines.
• Localized within alveolar bone proper.

128. INTERDENTAL SEPTUM
Consists of-
• Cancellous bone bordered by socket wall cribriform
plates (lamina dura/alveolar bone proper)
• Approximates teeth , facial and lingual cortical
plates.
• Narrow interdental space- septum has only one
cribriform plate.
• If roots are too close together an irregular
“window” appear in bone between adjacent roots.

129. INTERRADICULAR SEPTUM
The bony septum lying between the roots
OF multi rooted tooth is called inter
radicular septum

130. DETERMINING ROOT PROXIMITY-
RADIOGRAPHICALLY
• Mesiodistal angulation of the crest of the interdental
septum usually parallels a line drawn between the CEJ of
approximating teeth.
• Distance between crest of alveolar bone and CEJ in young
adults-
0.75 - 1.49(average 1.08)
• Distance increases with age (average2.81).

131. CLASSIFICATION

132. BASED ON SHAPE

136. BASED ON DEVELOPMENT
ENDOCHONDRAL
BONE
FORMED BY
REPLACEMENT OF
HYALINE CARTILAGE
WITH BONY TISSUE
OSSIFICATION OCCURS
IN TRUNK AND
EXTREMITIES
INTRAMEMBRANOUS
BONE
FORMED BY REPLACEMENT OF
SHEET LIKE CONNECTIVE TISSUE
MEMBRANE WITH BONY TISSUE
OSSIFICATION OCCURS IN
THE CRANIAL AND FACIAL
FLAT BONES OF SKULL ,
MANDIBLE AND CLAVICLE

138. BASED ON MICROSCOPIC
STRUCTURE

141. FUNCTIONAL ADAPTATION

142. RADIOGRAPHIC APPEARENCE
TYPE 1
REGULAR INTERRADICULAR AND INTERDENTAL
TRABECULAE
HORIZONTAL AND LADDER LIKE ARRANGEMENT
COMMON IN MANDIBLE
TYPE 11
IRREGULARLY ARRANGED NUMEROUS DELICATE
INTERDENTAL AND INTERRADICULAR TRABECULAE
COMMON IN MAXILLA

145. KEVITT’S CLASSIFICATION
NORMAL
HYPERCALCEMICHYPOCALCEMIC

146. LINLOW IN 1970
CLASS I BONE
STRUCTURE
EVENLY SPACED
TRABECULAE
WITH SMALL
CANCELLATED
SPACES
CLASS II BONE
STRUCTURE
SLIGHTLY LARGER
CANCELLATED
SPACES
LESS
UNIFORMITY OF
THE OSSEOUS
PATTERN
CLASS III
BONE
STRUCTURE
LARGE MARROW
FILLED SPACES
BETWEEN BONE
AND
TRABECULAE

148. LEKHOLM AND ZARB IN 1985
QUALITY I
HOMOGENOUS
COMPACT BONE
QUALITY II
THICK LAYER OF
COMPACT BONE
SURROUNDING
DENSE TRABECULAR
BONE
QUALITY III
THIN LAYER CORTICAL
BONE SURROUNDING
DENSE TRABECULAR
BONE (FAVOURABLE
STRENGTH)
QUALITY IV
THIN LAYER OF
CORTICAL BONE
SURROUNDING LOW
DENSITY
BONE

150. MISCH BONE DENSITY

154. DEVELOPMENT

155. Both jaw bones start as small centers of endochondral ossification around
stomodaeum
Later, the teeth become separated from each other by the development of interdental
septa.

157. With the onset of root formation, inter radicular bone develops in multi rooted teeth.
When a deciduous tooth is shed, its alveolar bone is resorbed.
The size of the alveolus is dependent upon the size of the growing tooth
germ.
Resorption occurs on the inner wall of the alveolus while deposition occurs on the
outer wall.
The developing teeth therefore come to lie in a trough of bone called the Tooth Crypt.

160. The succedaneous permanent tooth moves into place developing from its own alveolar
bone from its own follicle
Mandibular basal bones begins mineralization at the exit of the mental
nerve of the mental foramen
Maxillary basal bone begins mineralization at the exit of the infraorbital nerve from the
infraorbital foramen

161. BONE REMODELLING

163. BONE REMODELLING COMPARTMENT

164. BMU
CONTENTS

171. MEDIATORS OF BONE REMODELLING

172. HORMONES
• PRODUCED IN RESPONSE TO HYPOCALCEMIA-STIMULATING BONE RESORPTION
• “DUAL EFFECT” OF RESORPTION & FORMATION
• BONE RESORPTION STIMULATED BY PTH (CONTINOUS SUPPLY) SYNTHESIS OF RANKL
• INTERMITTENT DOSE: STIMULATE FORMATION OF BONE BY INCREASE IN GROWTH
FACTORS AND DECREASE ISN APOPTOSIS OF OSTEOBLASTS
PARATHYROID
HORMONE

173. • SECRETED WHEN THE BLOOD CALCIUM LEVEL RISE
• INHIBITS BONE RESORPTION- PROMOTE CALCIUM SALT CALCIUM LEVELS
• AS BLOOD CALCIUM FALLS: CALCITONIN RELEASE WANES
• REDUCE ACTIVITY OFOSTEOCLASTS
CALCITONIN

174. COUPLING
• The interdependency of osteoblasts and osteoclasts in
remodelling is called COUPLING
• The bone matrix laid down by the osteoblast is non-
mineralized OSTEOID.
• While new osteoid is being deposited the older
osteoid located below the surface becomes
mineralized as the mineralization front advances.

175. MARKERS OF BONE TURNOVER

176. MARKERS OF BONE TURNOVER

177. MARKERS OF BONE
TURNOVER
SERUM MARKERS
(BONE FORMATION)
ALK PHOSPHATASE
OSTEOCALCIN
PROCOLLAGEN I
EXTENSION PEPTIDE
URINARY MARKERS
(BONE RESORPTION)
URINE CALCIUM, URINARY
HYDROXY PROLINE URINE
N,C TELOPEPTIDE URINE
PYRIDINOLINE

178. BONE LOSS IN VARIOUS CONDITIONS
• Bone destruction caused by extension of gingival inflammation.
• Bone destruction caused by trauma from occlusion.
• Bone destruction caused by systemic disorders-
• Osteitis fibrosa cystica
• Paget’s disease
• Fibrous dysplasia
• Osteopetrosis
• Osteoporosis
• Scleroderma
• Malignancy

183. BONE DESTRUCTION BY SYSTEMIC DISORDERS

184. OSTEITIS FIBROUS CYSTICA

185. PAGET’S DISEASE FIBROUS DYSPLASIA

186. OSTEOPETROSIS OSTEOPOROSIS

187. FACTORS DETERMINING BONE MORPHOLOGY
• The thickness, width and crestal angulation of the interdental septa.
• The thickness of the facial and lingual alveolar plates.
• The presence of fenestrations and dehiscence.
• The alignment of the teeth.
• Root and root trunk anatomy.
• Root position within the alveolar process.
• Proximity with another tooth surface.

189. EXOSTOSIS
• These are outgrowths of bone of varied size and shape.
• They can occur as small nodules, large
• nodules, sharp ridges, spike-like projections or
• any combination of these.
• In rare cases, found to develop after the
• placement of free gingival grafts.

191. TRAUMA FROM OCCLUSION
• May cause a thickening of the cervical margin of alveolar bone or a change in the
morphology of bone (eg. angular defects, buttressing bone) on which inflammatory
changes will later be superimposed.

192. BUTTRESSING BONE FORMATION (LIPPING)
• Bone formation sometimes occurs in an attempt to buttress bony trabaculae
weakened by resorption.
• When it occurs within the jaw, termed Central buttressing bone formation.
• When it occurs on the external surface, termed Peripheral buttressing bone
formation.
• The latter may cause bulging of the bone contour, termed as Lipping, which
sometimes accompanies the production of osseous craters and angular defects.

193. GINGIVAL
SWELLING IN
RELATION TO
21
IOPA
SHOWING
INTERDENTAL
SPACING
THICKENED LABIAL CORTEX
ELEVATED FROM TOOTH SURFACE
THINNED LABIAL SURFACE FROM
BONE GRAFT IN PLACE

194. FOOD IMPACTION
• Interdental bone defects often occur where proximal contact is abnormal or absent.
• Pressure and irritation from food impaction contribute to the inverted bone
architecture.
• Poor proximal relationship may result from a shift in tooth position because of
extensive bone destruction preceding food impaction.

196. AGGRESSIVE PERIODONTITIS
• Vertical or angular pattern of alveolar bone
• destruction is found around the first molars.
• The cause of the localized bone destruction is unknown.

198. FENESTRATION AND DEHISCENCE
• Fenestrations - isolated areas in which the tooth is denuded of bone and the root surface is
covered only by periosteum and overlying gingiva.
Dehiscence - When the denuded areas extend through the marginal bone.
• Occurance - on approximately 20% of the teeth.
• Occur more often on the facial bone than on
• the lingual bone.
• More common on anterior teeth than on
• posterior teeth, and are frequently bilateral.
• Important because they complicate the outcome of periodontal surgery.

200. BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE
• Periodontal disease alters the morphologic features of the bone, in addition to reducing bone height.
• An understanding of its nature and pathogenesis is essential for effective diagnosis and treatment.
• Horizontal bone loss
• Bone deformities
• Vertical or angular defects
• Osseous craters
• Bulbous bone contours
• Reversed architecture
• Ledges
• Furcation involvement

201. BONE DEFORMITIES
(OSSEOUS DEFECTS)
• Different types of bone deformities seen in periodontal disease.
• Presence may be suggested on radiographs.
• Careful probing and surgical exposure of the areas required to determine their exact
nature.

202. HORIZONTAL BONE LOSS
Most common pattern of bone loss in periodontal disease.
Bone is reduced in height.
Bone margin remains approximately perpendicular to the tooth surface.
The interdental septa and facial and lingual plates are affected, but not necessarily to
an equal degree around the same tooth.

204. VERTICAL OR ANGULAR DEFECTS
• Occur in an oblique direction, leaving a hollowed-out trough in the bone along side the root;
the base of the defect is located apical to the surrounding bone.
• Angular defects are classified on the basis of the number of osseous walls, into one, two or
three walls.
• The number of walls in the apical portion of the defect may be greater than that in its occlusal
portion, termed as Combined osseous defect.
• Vertical defects occurring interdentally can generally be seen on the radiograph, although
thick, bony plates sometimes may obscure them.
• Angular defects can also appear on facial and lingual or palatal surfaces but are not seen on
radiographs.

207. Infrabony defects.
A.One-wall intrabony defect.
B. Two-wall intrabony defect.
C. Three-wall intrabony defect.

208. • Surgical exposure is the only way to determine the presence and configuration of vertical osseous
defect.
• Vertical defects increase with age.
• Vertical defects detected radiographically - most often appear on the distal and mesial surfaces.
• Three wall defects are more frequently found on the mesial surfaces of upper and lower molars.
• Originally called an Intrabony defect.
• Appears most frequently on the mesial aspects of second and third maxillary and mandibular molars.
• The one wall vertical defect is also called a Hemiseptum.

209. OSSEOUS CRATERS
• Concavities in the crest of the interdental bone confined within the facial and the
lingual walls.
• Found to make up about one third (35.2%) of all defects and about two thirds (62%)
of all mandibular defects.
• Occur twice as often in posterior segments than in anterior segments.

211. • Reasons for the high frequency of interdental craters are-
• Interdental area collects plaque and is difficult to clean.
• The normal flat or even concave faciolingual shape of the interdental septum in
lower molars may favor formation.
• Vascular patterns from the gingiva to the center of the crest may provide a pathway
for inflammation.

212. BULBOUS BONE CONTOURS
• Bony enlargements caused by exostoses , adaptation to function or buttressing
bone formation.
• Found more frequently in the maxilla than in the mandible.

214. REVERSED ARCHITECTURE
• Loss of interdental bone, including the facial and lingual plates, without
concomitant loss of radicular bone, thereby reversing the normal architecture.
• More common in the maxilla.

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

217. FURCATION INVOLVEMENT
• Invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease.
• The number of furcation involvements increases with age.
• Classified as grades I, II, III and IV, according to the amount of tissue destruction.
• Grade I is incipient bone loss.
• Grade II is partial bone loss (cul-de-sac).
• Grade III is total bone loss with through and through opening of the furcation.
• Grade IV is similar to Grade III, but with gingival recession exposing the furcation to view.
• The diagnosis is made by clinical examination and careful probing with a specially designed
probe.

220. THERAPEUTIC CONSIDERATIONS
• Many osseous grafting materials are currently available.
• Has been used in periodontal surgery since the 1970’s.
• Involves a surgical procedure to place bone or bone substitute material into a
bone defect with the objective of producing new bone and possibly the
regeneration of periodontal ligament and cementum.

222. AUTOGRAFTS
• Utilizes the patient’s bone, obtained from intraoral or extraoral sites.
• Best materials for bone grafting.
• Very well accepted by the body and may produce the fastest rate of bone growth.
• Potential risk of additional discomfort and a secondary procedure.
• Patient is assured of protection from disease transmission and/or immune reaction.

224. ALLOGRAFTS
• Available either demineralized or non-demineralized.
• Includes growth factors which are osteoinductive.
• Induces bone growth and provide an environment that increases the body’s
regenerative process.

226. XENOGRAFTS
• Obtained from animal sources; usually cows and/or pigs.
• Include processed animal bone or growth proteins.
• Risk of disease transmission and/or rejection is reduced by processing.

228. SYNTHETIC BONE GRAFTING MATERIALS
• Examples - Natural and synthetic hydroxyapatites, Ceramics, Calcium carbonate
(natural coral), Silicon-containing glasses and Synthetic polymers.
• No risk of disease transmission or immune system rejection.
• Creates an environment that facilitates the body’s regenerative process.

230. BIOLOGICALLY MEDIATED STRATEGIES
• Include materials, such as enamel matrix proteins, that can be premixed with vehicle
solution.
• Intended as an adjunct to periodontal surgery for topical application onto exposed
root surfaces or bone.
• Leaves only a resorbable protein matrix on the root surface, which makes bone
more likely to regenerate.
• Initiates a cascade of events leading to the differentiation of progenitor cells into
phenotypes involved in periodontal regeneration.

231. NEW DEVELOPMENTS
Alveolar distraction
• Alveolar bone distraction recently was introduced as an alternative to bone grafting for ridge augmentation of
traumatically induced, limited alveolar defects.
Micro-osteoperforation
• Bone remodeling allows greater movement of the teeth. The previous highly invasive technique can be
replaced with small, shallow micro-osteoperforations in the alveolar bone without the need for soft tissue
flaps, bone grafting or suturing.

234. CONCLUSION
• The alveolar processes develop and undergo remodeling with the tooth formation
and eruption- Tooth dependent bony structure.
• Although its constantly changing its internal organization, it retains the same form
from childhood through adult life.
• The coupling of bone resorption with bone formation constitutes one of the
fundamental principles by which bone is remodeled throughout its life.

235. REFERENCE
Newman, Takei, Klokkevold, Carranza 2007. Clinical Periodontology.
10th Edition.
Berkovitz, Holland, Moxham 2002. Oral Anatomy, Histology and
Embryology. 3rd Edition.
Kumar 2007. Orban’s Oral Histology and Embryology. 12th Edition

236. REFERENCE
Ten Cate. Oral Histology : Development, Structure and Function.
Shafer’s. Oral Pathology.