BONE

2. ALVEOLAR BONE IN STATE OF
FLUX
GUIDED BY PRESENTED BY
DR.NEEMA SHETTY DR.JINAL PATEL
DR.ADITI MATHUR
DR.ASHISH BALI
DR.PRITISHCHANDRA PAL

3. CONTENTS:
• INTRODUCTION OF BONE
• CLASSIFICATION OF BONES
• COMPOSITION OF BONE
• DEVELOPMENT OF BONE
• RESORPTION OF BONE
• BONE HISTOLOGY
• SKELETAL HOMEOSTASIS
• INTRODUCTION OF ALVEOLAR BONE
• GROSS MORPHOLOGY OF ALVEOLAR BONE
• CLASSIFICATION OF ALVEOLAR BONE
• BLOOD AND NERVE SUPPLY OF ALVEOLAR BONE
• FUNCTIONS OF ALVEOLAR BONE
• BONE REMODELING
• ALVEOLAR BONE IN STATE OF FLUX
• HEALING OF ALVEOLAR BONE AFTER EXTRACTION
• CLINICAL CONSIDERATION
• AGE CHANGES
• CONCLUSION
• REFERENCES

4. INTRODUCTION:
Bone is a living tissue , which makes up the body skeleton & It is one of the
hardest structures of the animal body.
Functions of bone:
 Provide shape &support of the body.
 Provide site for attachment for the tendon & muscles.
 Protects the vital organs of the body.
 Serves as a storage site for minerals & provides the medium , the marrow for
the development &storage of blood cells.

5. CLASSIFICATIONS OF BONES:
1).Based on shape:
 Long bone
 Short bone
 Flat bone
 Sesamoid bone
2).Based on Development:
 Endochondrial bone formation
 Intramembranous bone formation
3).Based on microscopic structures:
 Mature bone:
-Compact bone
-Cancellous bone
 Immature woven bone

6. COMPOSITION OF BONE:
◦ Bone is a connective tissue composed of cells, fibers & ground substances.
◦ Intercellular substances of bone are:
Inorganic components: Organic components:
 Minerals: Hydroxyapatite crystals,
 Carbonate content
 Ions : Ca+2 , PO4- , OH- , Collagen Non
CO3- , Citrate , MG+2 , Protein Collagenous
Na+ , K+ , F- , Fe+2 , protein
Zn+2 , Cu+2 , Al+3 ,Pb+2 ,St , Si , B .
Collagen protein :
 Type 1 collagen(95%) is the principle collagen in mineralized bone .
 Type 1,3,5,12 collagen present in alveolar bone .
 Type 3 &12 collagen produced by fibroblast during formation of PDL .
 Type 5 & 12 collagens are expressed by osteoblasts .
Functions of collagen :- Type 1&5 provide basic structural integrity of connective tissue.
Provide resiliency to connective tissue & resist fractures. Functions of collagen.

7. 2.Non collagenous proteins : Comprise the remaining 10% of the total organic content of bone
matrix.
Produced by: bone cells .
 Albumin derived from blood & incorporated into bone matrix.
 Osteocalcin : Secreted by osteoblasts & regulated by vitamin D3 and parathyroid hormone.
Also play a role in bone resorption.
 Osteopontin : Inhibiting hydroxyapatite crystal growth.
 Bone sialoprotein: Initiating mineral crystal formation in vivo.
 Osteonection : Play a role in the regulation of cell adhesion , proliferation & modulation of
cytokine activity & initiating hydroxyapatite crystal formation.
 Proteoglycans : Binding to various growth factors as co-receptors & cell repair.

8. DEVELOPMENT OF BONE:
Intramembranous bone Formation

9. Endochondral bone formation:

11. cells:
 Osteogenic precursor cells
 Osteoblasts
 Osteoclasts
 Osteocytes
 Mesenchymal stem cells
 Hematopoietic elements of bone marrow
 Osteogenic precursor cells : The stem cell population that give rise to osteoblasts are
termed as Osteoprogenitor cells.
◦ They are fibroblast-like cells, with an elongated nucleus and a few organelles.
◦ Their life cycle may involve up to about eight cell divisions before reaching the osteoblast
stage.
◦ They reside in the layer of cells beneath the osteoblast layer, in the periosteal region, in the
periodontal ligament or in the marrow spaces.

12.  Osteoblasts : Osteoblasts are mononucleated cells responsible for the
synthesis and secretion of the macromolecular organic constituents of
bone matrix. These cells are derived from osteoprogenitor cells of
mesenchymal origin, which are present in the bone marrow and other
connective tissues. Periosteum also serves as an important reservoir of
osteoblasts, particularly during childhood growth, after skeletal fractures
or with bone forming tumors.
Morphology:
Basophillic ,slightly
flattened cells &nucleus
:eccentric & away from
the adjucent bone
surfaces.
It produces organic
matrix of bone which
primarily consist of
type:I collagen.
Found on forming
surfaces of growing or
remodeling bone.
Also produce non
collagenous protein on a
osteoblast surface .They
participate in regulating
mineral deposition.
Contains : Bundles of
actin & myosin
-cytoskeletal proteins .
Which are associated
with maintainance of
cell shape , attachment
&motility.

13. Osteoblast formation:
◦ Osteoblasts are derived from undifferentiated pluripotent mesenchymal cells.
◦ Osteoprogenitor cells differentiate & developed into:
◦ Osteoprogenitor cells express transcription factors Runx-2:which is essential for
osteoblastic differentiation.
• Present in bone marrow ,
periosteum , endosteum.
• Differentiate into osteoblast.
• Under influence of systemic &bone
derived growth factors.
Determined
osteogenic
precursor cells
• Represent :mesenchymal cells.
• Present in : other organs & tissues.
• Differentiate into osteoblast when
stimulated.
Inducible
osteogenic
precursor cells

14. ◦ Osteoblast located on bone surfaces & differentiated in to
Bone lining cells:
• Elongated cells
• Covers the surface of bone tissue.
• No synthetic activity.
• Lack of capacity for migration
&proliferation.
Osteocytes
Functions of bone lining cells:
• Formation of new bone via synthesis of various proteins
&polysaccharides.
• Regulation of bone remodeling &mineral metabolism.
• Secrete type : I collagen &small amounts of type : V collagen ,
osteonectin , osteopontin , RANKL , osteoprotegerin ,
proteoglycans , BMP.
Regulation : by hormones & proteins secreted by hematopoietic bone marrow
cells & bone cells.

15. OSTEOCYTES:
◦ Shape : Stellate shaped cells
◦ Embedded with in mineralized bone matrix in compartment known as lacunae.
◦ Maintain a network of cytoplasmic projections extend through cylindrical encased
compartment refered as a canaliculi.
◦ Osteoblasts produce the extracellular matrix, osteoid. As the osteoblasts form the
bone matrix, they get entrapped within the matrix they secrete, and are called
osteocytes.
◦ The number of osteoblasts that become osteocytes, depends on the rapidity of
bone formation.
assist in modulating anabolic and catabolic events with in bone
Mechanical signals osteocyte Biomechanical mediators

17. Osteoclasts:
◦ The word "osteoclast" is derived from the Greek words for "bone and broken".
Osteoclast is a type of bone cell chat removes bone tissue by removing the
mineralized matrix.These cells are variable in shape due to their motility. The
cytoplasm of the osteoclast shows acid phosphatase containing vesicles and
vacuoles.
◦ Osteoclasts lie in resorption bays called Howship's lacunae.
The presence of acid
phosphatase distinguishes the
osteoclast from other
multinucleated giant cells.
Cathepsin containing
vesicles and vacuoles
are present close to the
ruffled border
indicating resorptive
activity of these cells.
Osteoclast is a large cell approximately
40-100 um in diameter with 15 to 20
closely packed nuclei. Osteoclasts with
many nuclei resorb more bone than
osteoclasts with few nuclei.
These cells are variable in shape due to
their motility. The cytoplasm of the
osteoclast shows acid phosphatase
containing vesicles and vacuoles

18. Osteoclast formation:
Formation requires :
presence of RANKL ligand
& M-CSF
M-CSF provide signals
required for
proliferation
Enhances osteoclastic
activity by preventing
osteoclast apoptosis.

19. Enzymes of osteoclasts:
1.Cathepsin-K:
◦ It is a collagenolytic enzyme.
◦ Degrades major amount of Type 1 Collagen and other non-collagenous proteins.
2.Matrix metalloproteinase(MMPs):
◦ MMP-9 (Collagenase B) – Osteoclast migration.
◦ MMP-13- osteoclast differentiation.
3. Tartarate resistant acid phosphatase ( TRAP):
◦ TRAP is synthesized as a latent inactive proenzyme.
◦ This active enzyme plays a role in bone resorption inside and outside the osteoclast cell.
◦ In osteoclasts, TRAP is localized within the ruffled border area.

20. BONE RESORPTION:
◦ It is the process of removal of mineral and organic components of extracellular
matrix of bone by osteolytic cells called osteoclasts.
◦ SEQUENCE OF EVENTS OF BONE RESORPTION:
First phase : Formation of osteoclast
progenitors in the hematopoietic
tissues.
Third phase - Activated osteoclasts
resorbing the bone.
Second phase : Activation of osteoclasts
osteoclasts at the surface of
mineralized bone.

21. Attachment of osteoblast to the mineralized
surface of the bone.
Creation of sealed acidic environment
through action of proton pump , which
demineralize the bone & expose the organic
matrix.
Degradation of exposed organic matrix to it’s
constituent amino acids by the action of
released enzymes , such as ACID
PHOSPHATASE & CATHEPSIN.
The natural MMPs also play a role
during the organic matrix
degradation.
Sequestring of mineral ions &
amino acids with the osteoclasts.
After completing resorption ,
osteoclast either undergo apoptosis
or perform a further round of
resorption.

22. BONE FORMATION & RESORPTION COUPLING:

23. BONE HISTOLOGY:
◦ Mature bones : consists of dense outer sheet of
compact bone &central
medullary cavity.
1.Periosteum : Outer aspect of compact bone is surrounded by a condensed
fibrocollagen layers.
OUTER LAYER :Dense ,
irregular connective
tissue termed as
FIBROUS LAYER.
INNER LAYER : Next to the
bone surface consisting of
bone cells , their precursor
cells & a rich vascular
supply.
Active during fetal development
& important in the repair of
fractures.

24. • 2.Endosteum: Inner surface of the compact and
cancellous bone are covered by a thin cellular layer
called as a ENDOSTEUM.
• In resting adult bone ,osteoblasts & osteoprogenitor
cells : present on the endosteal surfaces.
• Act as a reservoir of new bone forming cells for
remodeling.

25. Lamellae arranged
in parallel layers
surrounding the
bony surface &
called
CIRCUMFERENTIA
L LAMELLAE.
Deep to the
circumferential
lamellae , the
lamellae arranged as
a small concentric
layers around a
central vascular
canal.
Osteon/Haversian
system : Vascular
canal and
concentric
lamellae together
is known as
osteon.

26. Bone marrow:
◦ Consists of hematopoietic tissue islands , stromal cells & adipose cells.
◦ Major hematopoietic organ : primary lymphoid tissue responsible for the
production of erythrocytes , granulocytes , monocytes , lymphocytes , platelets .
• RED BONE MARROW:
• Consist mainly of
hematopoietic tissue.
• Erythrocytes , leukocytes
and platelets arise in red
marrow .
• At birth , all bone marrow is
red.
• YELLOW BONE MARROW:
• Mainly made up of
adipocytes.
• With age more &more red
bone marrow converted into
yellow bone marrow.
• Only around half of adult
bone marrow is red.

27. In case of several blood loss: the body
can convert yellow marrow back to red
marrow to increase blood cell
production.

28. ◦ Cells : 1). Fibroblasts
2).Macrophages
3).Adipocytes
4).Osteoblasts
5).Osteoclasts
6).Endothelial cells
Stem cells : Give rise to the LEUCOCYTES ,
ERYTHROCYTES , PLATELETS .
• FUNCTIONS : To provide locomocation ,
organ protection & mineral homeostasis .
• Influence the balance between bone
resorption &bone formation.
• Provide mechanical strength & allow
movement.

29. Mechanical properties :
◦ Bone is highly dynamic tissue & has capability to adapt based on physiological
needs.
◦ Bone adjusts its mechanical properties according to metabolic & mechanical
requirement.
◦ Hydroxyapattite regulates both :- Elastic stiffness.
-Tensile strength of bone.
Bone tissue responds to loading:
By increasing matrix synthesis , altering
composition , organization &mechanical
properties.
Mechanical deformation of the
bone matrix induces electric
potentials that stimulates
osteoclastic resorption.

30. SKELETAL HOMEOSTASIS:
◦ Healing
1).Repair
2).Regeneration
It includes both
regeneration &
repair
depending on
the nature of the
injury .
REPAIR :Tissue injury occurs , healing leads to
formation of a tissue that differs in morphology ,
composition , functions of a original tissue.
• Phase:1).Inflammation-begins immediately after
tissue injury &lasts up to 2 weeks.
• Formation of blood clot.
• Phagocytosis of damaged tissues.
• Cells from myeloid & mesenchymal cell begin
differentiate in to osteoblasts.

31. Phase: 2). Repairative – Formation of soft callus.
• Which is slowly mineralized &form hard callus. It is
composed of immature woven bone.
• Occurs approximately 6-12 weeks from the time of
bone injury.
Phase :3).Remodeling- Bone matrix and cartilage are
remodeled into mature bone.
Woven bone Mature lamellar bone
It requires months from the time of bone injury.

32. 2.REGENERATION:
◦ Healing process that results in complete restoration of morphology ,
composition & functions .
◦ Coupling of bone formation and resorption occur in a basic multicellular
unit.(BMU)
• Theraputic strategies to promote
bone regeneration:
• Bone grafts
• Epithelial occlusal barrier
membranes.
• Anabolic agents.
• Growth factors.

33. Bone resorption by osteoclasts occurs first over a period of 3-4
weeks , along with cellular signaling to promote osteoblasts
then form bone for a period of 3-4 months.
Conditions can alter bone
Homeostasis :
• Cancer
• Menopause
• Medications
• Genetic conditions
• Nutritional deficiency infection
• Vit D deficiency

34. ALVEOLAR BONE:-
◦ Alveolar bone is the portion of the maxilla & mandible that forms & support
tooth socket.
◦ It is formed when the tooth erupts ,in order to provide the osseous attachment
to the forming periodontal ligaments ;it disappear gradually after the tooth lost.
◦ GROSS MORPHOLOGY OF ALVEOLAR BONE :
Anatomically, no distinct boundary exists
between the body of the maxilla or the
mandible and their respective alveolar
processes.
In the anterior part of the maxilla, the palatine process fuses with
the oral plate of the alveolar process. In the posterior part of the
mandible, the oblique line is superimposed laterally on the bone
of the alveolar process.

35. As a result of its adaptation to
function, two parts of the alveolar
process can be distinguished,
1). The alveolar bone proper
2).The supporting alveolar bone.
1.THE ALVEOLAR BONE PROPER : The alveolar bone proper consists partly of
lamellated and partly of bundle bone and is about 0.1-0.4 mm thick. It
surrounds the root of the tooth and gives attachment to principal fibers of the
periodontal ligament.

36. • Bundle bone is that bone in which the principal
fibers of the periodontal ligament are anchored. The
term 'bundle was chosen, because, the bundles of
principal fibers continue into the bone as Sharpey's
fibers.
• The alveolar bone proper, which forms the inner wall
of the socket is perforated by many openings that
carry branches of the interalveolar nerves and blood
vessels into the periodontal ligament, and it is
therefore called the CRIBRIFORM PLATE.

37. 2).SUPPORTING ALVEOLAR BONE :
Consists of two parts A).Cortical plate
B).Spongy bone
Cortical plates consist
of compact bone
&form outer &inner
plates of alveolar
process.
The cortical plates ,
continuous with the
compact layers of the
maxillary and
mandibular body.
Thinner in maxilla.
Thickest in pre molar &
molar region of mandible .
Especially on buccal side.

38. • Bone underlying the gingiva is
the cortical plate.
Both cribriform and cortical plate
are compact bone and separated
by spongy bone.
• In the region of anterior teeth of
both jaws ,supporting bone is thin.
No spongy bone is found here &
cortical plate fused with alveolar
bone proper.

39. Bone between the
teeth is called
interdental septum and
is composed entirely of
cribriform plate.
The interdental and
interradicular septa contain
the perforating CANALS OF
ZUCKERKANDL AND
HIRSCHFELD (nutrient
canals) which house the
interdental and inter-
radicular arteries, veins,
lymph vessels and nerves.
The interdental and
interradicular septa
contain the perforating
CANALS OF
ZUCKERKANDL AND
HIRSCHFELD (nutrient
canals) which house
the interdental and
inter-radicular arteries,
veins, lymph vessels
and nerves.

40. SPONGY BONE :
◦ Spongy bone fills the area between the cortical plates and the alveolar bone
proper.
◦ It contains trabeculae of lamellar bone.
◦ These are surrounded by marrow that is rich in adipocytes and pluripotent
mesenchymal cells.
◦ The trabeculae contain osteocytes in the interior and osteo-blasts or
osteoclasts on the surface.
◦ These trabeculae of the spongy bone buttress the functional forces to which
alveolar bone proper is exposed.
◦ The cancellous component in maxilla is more than in the mandible.

41. Interdental septum:
• Bony partition that separate the adjacent alveoli.
• Coronally septa is thin and consists of only fused inner
cortical plates.
• Apically septa is thicker and contain intervening
cancellous bone.
• Mesiodistal angulation of interdental septum is parallel
to line drawn between CEJ of approximating teeth.
If interdental space is
narrow, septum may
consist of only
cribriform plate.
If roots are too close together, an Irregular window
can appear in the bone between adjacent roots.

42. The shape of the Interdental bone is a function of the
tooth form and embrasure width.
• The more tapered the tooth, the more pyramidal is the
bony form.
• The wider the embrasure, the more flattened is the
interdental bone mesiodistally and buccolingually.

43. OSSEOUS TOPOGRAPHY:
Normally: prominence of the roots
will lie intervening vertical
depressions that taper toward the
margin.
On the labial version- margins of the labial bone
is thinned to a knife edge & presents an
accentuated arch in the direction of the apex.
On the lingual version: the margins are blunt &
rounded & horizontal rather than arcuate.

44. CLASSIFICATION OF ALVEOLAR BONE:
1. BASED ON THE FUNCTIONAL ADAPTATION:
2. BASED ON THE RADIOGRAPHIC APPEARANCE:
2. BASED ON HISTOLOGICAL FEATURES:
A. Alveolar bone proper.
B. Supporting alveolar bone
Type 1- regular interradicular and interdental trabeculae
horizontal in a ladder like arrangement. Common in mandible.
Type 2- irregularly arranged numerous , delicate interdental and
interradicular trabecular. Common in maxilla.
 MATURE BONE -
A . Compact Bone
B . Cancellous Bone
 IMMATURE BONE -
A . Woven bone

45. Blood & nerve supply of Alveolar bone:
• The vascular supply to the alveolar
bone is derived from the inferior and
superior alveolar arteries of maxilla
and mandible, venous drainage
accompanies the arterial supply.
Vascular supply:
• The nerve supply to the alveolar bone
is derived from the anterior , middle
and posterior superior alveolar nerves
for maxilla and branches from inferior
alveolar nerve for mandible.
Nerve supply:

46. Functions of Alveolar bone :
◦ Houses the roots of the teeth.
◦ Anchors the roots of teeth to the alveoli, which is achieved by the insertion of
Sharpey’s fibres into the alveolar bone proper.
◦ Helps to move the teeth for better occlusion.
◦ Helps to absorb and distribute occlusal forces generated during tooth contact.
◦ Supplies vessels to the periodontal ligament.
◦ Houses and protects developing permanent teeth while supporting primary
teeth.
◦ Organizes eruption of primary and permanent teeth.

47. BONE REMODELING:
◦ The process by which overall shape and size of bones is established is referred to
as bone remodeling or turnover.
◦ It occurs in discrete, focal areas involving groups of cells called bone remodeling
or basic multicellular units.
◦ During this phase bone is formed along the periosteal surface and destroyed
along the endosteal surface.
◦ The status of bone represents the net result of a balance between the two
processes-Coupling' of bone resorption and formation.
◦ FUNCTIONS:
◦ To prevent the accumulation of damaged and fatigued bone by regenerating
new bone.
◦ To allow bone to respond to changes in mechanical forces.
◦ To facilitate mineral homeostasis.

48. Sequence of Events:
◦ 1).ACTIVATION STAGE :
◦ Cells of the osteoblast interact with hematopoietic cells to initiate osteoclast
formation.
◦ Structual damage occur.
2).RESORPTION STAGE :

49. 3).Reversal stage :
3).REVERSAL STAGE :

50. REGULATORS OF BONE REMODELING :
◦ BONE PROTECTORS:
• CALCITONIN
• BISPHOSPHONATES
• STATINS
• OSTEOPROTEGRIN
• INTERFERON GAMMA
• GLUCOCORTICOIDS
• INDOMETHACIN/ASPIRIN
• IL-1 RECEPTOR
ANTAGONIST
• ESTROGEN
• LEPTIN

51. BONE RESORBERS : • PARATHYROID HORMONE
• VITAMIN D3
• IL-1
• IL-6
• TNF-a AND b
• COLONY STIMULATING
FACTORS
• PROSTAGLANDINS
• RANKL/OPG-L/TRANCE
• BACTERIAL PRODUCTS

52. MEDIATORS OF BONE REMODELING :
◦ 1). PARATHYROID HORMONE :
◦ Produced by parathyroid glands in response to hypocalcemia , stimulating bone
resorption .
◦ Continuous supply of PTH stimulates bone resorption through the synthesis of
RANKL on the surface of osteoblast.
◦ While at intermittent doses of PTH , stimulate bone formation , associated with
increase growth factors & decrease apoptosis of osteoblasts.
2). CALCITONIN :
o Secreted when blood calcium level rise.
o Inhibit bone resorption , promotes calcium salt deposition in bone matrix ,
effectively reducing blood calcium level.
o Also reduces osteoclastic activity.

53. 3).Vit –D metabolites :
◦ Major active metabolite of vit – D IS 1,25-Dihydroxychole- calciferol.
• Increase intestinal absorption
of calcium , phosphate .
• Enhance bone mineralization.
Bone formation:
• By differentiation of committed
progenitor cells into mature cells.
Bone resorption:

54. Estrogen receptors:
• Present on osteoblasts , osteocytes
&osteoclasts.
• Favors bone formation & inhibit
resorption.
• Increase the levels of OPG.
Growth Hormones:
• Act directly on the osteoblasts , stimulating
their activity& increasing synthesis of collagen
, osteocalcin & alkaline phosphatase.
• Increase synthesis of IGF I & II by osteoblasts ,
which stimulate proliferation &
differentiation of osteoblasts.
Glucocorticoids:
Inhibit the synthesis of IGF –I by osteoblasts &
suppress BMP II :Which are essential for the bone
formation.

55. Serum marker of bone resorption :
1.Urine calcium
2.Urine hydroxyproline
3.Collagen cross link fragments
Serum marker of bone formation :
1.Alkaline phosphatase
2.Osteocalcin
3.Procollagen I extension peptide

56. ALVEOLAR BONE IN STATE OF FLUX:
Teeth migrate adaptively to crown attrition. The migration rate seems to peak during growth
and declines afterwards without ceasing completely.
To accommodate the movement, the surrounding bone has to deform in front of and behind
the migrating teeth.
This deformation is quite assimilable to the process known as modeling in bone physiology.
During modeling one side of a bone is resorbed by osteoclasts while bone is deposited by
osteoblasts on the opposite side.

57. This permits progressive drift of the bone surfaces and ultimately the gross modification of the
organ shape.
During tooth migration this process is complicated by the necessary preservation of the
periodontal ligament anchorage to bone.
On the side of the socket in the direction of migration (resorbing side), the alveolar wall is de-
formed through asynchronous cycles of resorption- formation in localized foci during which
the anchorage is temporarily lost and reformed without functional disturbance.

58. HEALING OF ALVEOLAR BONE AFTER EXTRACTION :
IMMEDIATELY
AFTER
EXTRACTION
• Immediately after the removal of the tooth from the socket, blood fills
the extraction site.
• Organization of the clot begins within the first 24 to 48 hours with
dilation and engorgement of blood vessels within the periodontal
ligament remnants , followed by leukocytic migration and formation
of fibrin layer.
1ST-3rd WEEK
• The clot forms a temporary scaffold upon which
inflammatory cells migrate.
• Epithelium at the wound periphery grows over the surface
of the organizing clot and the osteoclast accumulate along
the alveolar bone crest.
• Angiogenesis proceeds in the remnants of the periodontal
ligaments.

59. 3rd-4thWEEK
The clot continues to get organized through the fibroplasia and
new blood vessels that begin to penetrate towards the center of
the clot.
-Trabeculae of the osteoid slowly extend into the clot from the
alveolus, and the osteoclastic resorption of the cortical margin
of the alveolar socket is more distinct.
The extraction socket is filled with the granulation tissue and
poorly calcified bone forms active bone remodeling by
deposition and resorption continue for several more weeks.
4th-6th WEEK

60. CLINICAL CONSIDERATION :
1. NORMAL VARIATIONS IN ALVEOLAR BONE
2. FENESTRATION AND DEHISCENCE
3. EXOSTOSES.
4. TRAUMA FROM OCCLUSION
5. BONE LOSS AND BONE DESTRUCTION PATTERNS CAUSED BY PERIODONTAL
DISEASES
6. BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS.

61. NORMAL VARIATIONS IN ALVEOLAR BONE
FENESTRATION AND DEHISCENCE:

62. TRAUMA FROM OCCLUSION
◦ When occlusal forces exceeds the adaptive capacity and reparative capacity of
the periodontal tissues, tissue injury results i.e trauma from occlusion.
◦ Persistent trauma from occlusion results in funnel-shaped widening of the crestal
portion of the periodontal ligament with resorption of the adjacent bone.
◦ These changes, which may cause the bony crest to have an angular shape,
represent adaptation of the periodontal tissues aimed at "cushioning" increased
occlusal forces; however, the modified bone shape may weaken tooth support
and cause tooth mobility.

63. BONE LOSS AND BONE DESTRUCTION PATTERNS CAUSED BY
PERIODONTAL DISEASES
◦ The factors involved in bone destruction in periodontal disease are bacterial
plaque and host mediated.
◦ In patients with rapidly progressing diseases , bacterial microcolonies or
single bacterial cells have been found between collagen fibers and over the
bone surface, which suggests a direct effect.
◦ That result in the loss of collagen and alveolar bone and the deepening of the
periodontal pocket.

64. VARIOUS PATTERNS OF BONE DESTRUCTION
FURCATION INVOLVEMENT
VERTICAL /ANGULAR DEFECT
HORIZONTAL BONE
LOSS

65. BONE DESTRUCTIONS CAUSED BY SYSTEMIC DISORDERS:
◦ ENDOCRINE DISORDERS:
1).HYPERPARATHYRODISM :Endocrine abnormality in which there is an excess of
PTH.
-Bones appear quite radiolucent with thin cortices and hazy indistinct trabeculae.-
Thinning of the cortical boundaries- Density of the jaws is decreased.- Normal
trabecular pattern to ground glass appearance- Trabeculae are numerous small
randomly oriented- Loss of lamina dura.
 2).HYPERPITUTARISM: Results from hyperfunction of the anterior lobe of the
pituitary increases the production of the growth hormone.
 Enlargement of the mandible.
 Increase in the length of the dental arches. Thickness and height of the alveolar
process may increase.

66. 3).HYPERTHYRODISM:
Synonyms: Graves disease, Thyrotoxicosis.
• Excessive production of thyroid hormone.
• Generalized decrease in bone density.
4).HYPOTHYRODISM :
Synonyms; myxedema, cretinism.
• In sufficient secretion of thyroxin.
• Thinning of lamina dura.

67. 4).DIABETES MELLITUS:
• Bone size and bone mass are reduced.
• Contribution of advanced glycation end-products (AGES) to decreased
extracellular matrix production and inhibition of osteoblast differentiation.
6).CUSHING SYNDROME:
Due to excess secretion of glucocorticoids.
• Generalized osteoporosis.
• Granular bone pattern.
• Partial loss of lamina dura.

68. METABOLIC DISORDERS:
1).OSTEOPOROSIS:
Generalized decrease of bone mass.
• Imbalance between bone formation and resorption.
• Decrease in bone formation result in changes in trabecular architecture, volume of
trabecular bone, size and thickness of individual trabeculae.
• Trabeculae are thin and indistinct.(Diffuse granularity)
• Thinning of cortical boundaries.
• Lamina dura is thinned.

69. 2).HYPOPHOSPHATASIA:
Due to defective production are function of alkaline phosphatase.
• Jaws: generalized radiolucency of maxilla and mandible.
• Lamina dura is thin.
3).OSTEOPETROSIS:
Disorder of bone results from a defect in the differentiation and function of
osteoclasts.
• Increased density bilaterally symmetrical.
• Internal aspect of bane is radio-opaque.
• Entire bone is enlarged.
• Increased radio-opacity of jaws.
• Lamina dura is thicker than normal.

70. 4)HYPOPHOSPHETEMIA:
• Group of inherited conditions that produce renal tubular disorders resulting in
excessive loss of phosphorus.
• Osteoporotic jaws, granular trabecular pattern.
• Thinning of cortical boundaries.
• Lamina dura become sparse.

71. OHER SYSTEMIC DISORDERS:
Progressive systemic sclerosis
Sickle cell anemia
Leukemia
Thalassemia

72. AGE CHANGES:
Similar to those occurring in remainder of skeletal system.
Osteoporosis with ageing.
Decreased vascularity.
Reduction in metabolic rate and healing capacity.
Bone resorption may be increased or decreased.
More irregular periodontal surface.

73. CONCLUSION:
◦ The alveolar process develops and undergoes remodelling with the tooth
formation and eruption-tooth dependent bony structure.
◦ Although it is constantly changing its internal organization, it retains the
same form from childhood throughout adult life.
◦ The coupling of the bone resorption with bone formation constituents one
of the fundamental principles by which bone is remodelled throughout its
life.

74. REFERENCES:
◦ CARRANZA’S CLINICAL PERIODONTOLOGY, SOUTH ASIA SECOND
EDITION.
◦ MOLECULAR AND CELLULAR BIOLOGY OF ALVEOLAR BONE, PERIO 2000 ,
VOL24 , 2000 , 99-126.
◦ ALVEOLAR BONE AND THE ALVEOLAR PROCESS: THE SOCKET THAT IS
NEVER STABLE , PERIO 2000 , VOL 13 , 1997 , 76-90
◦ ORBAN’S DENTAL HISTOLOGY AND EMBRYOLOGY , 13TH EDITION
◦ PIYUSH SHIVHHARE ,1ST EDITION
◦ LINDHE CLINICAL PERIODONTOLOGY & IMPLANT DENTISTRY -7TH
EDITION
◦ SHAFERS, TEXTBOOK OF ORALL PATHOLOGY, 9TH EDITION.
◦ B D CHAURASIA’S HANDBOOK OF GENERAL ANATOMY, 4TH EDITION.
◦ ESSENTIALS OF CLINICAL PERIODONTOLOGY AND PERIODONTICS,
SHANTIPRIYA REDDY, 4TH EDITION