Alveolar bone in health and disease.

1. PRESENTED BY:
DR. HARDI GANDHI

3. WHAT IS BONE?
 Bone is a dynamic structure that is
adapting constantly to its
environment and they are essential
elements for locomotion, anti-gravity
support and life sustaining functions
such as mastication.
 It is remarkable for its hardness,
resilience & regenerative tissue.
 Highly Vascular.

4. Macroscopic structure
 Compact bone/cortical bone: Densely packed with organic ground substance and
inorganic salts, leaving only tiny spaces (lacunae) that contain the osteocytes.
 Usually limited to the cortices of mature bones (cortical bone) function is to
provide strength.
 Cancellous bone/spongy bone: Less dense & lies chiefly between cortices &
gives additional strength and supports the bone marrow.

7. Each osteon consists of a single central canal,
known as a haversian canal, surrounded by
concentric layers of calcified bone matrix.
Haversian canals allow the passage of blood
vessels, lymphatic vessels, and nerve fibers.
Each of the concentric matrix “tubes” that
surrounds a haversian canal is known as a
lamella.
HAVERSIAN CANAL :

8.  All the collagen fibers in a
particular lamella run in a single
direction, while collagen fibers in
adjacent lamellae will run in the
opposite direction.
 This allows bone to better
withstand twisting forces.

9. Concentric lamellae are arranged
concentrically around haversian canal.
 Interstial lamellae Lying in between intact
osteons . These fill the gaps between
osteons or are remnants of bone
remodeling.
Circumferential lamellae are found at the
outer and inner periphery of the cortex.
LAMELLAE

10. Spider-shaped osteocytes occupy
small cavities known as lacunae at
the junctions of the lamellae.
Hairlike canals called canaliculi
connect the lacunae to each other
and to the central canal.
 Canaliculi allow the osteocytes to
exchange nutrients, wastes, and
chemical signals to each other via
intercellular connections known as
gap junctions.

11.  These are oblique canals running at right
angles to the long axis of bone. they contain
neurovascular bundle.
 They connect the haversian canal with the
medullary cavity and surface of bone.
 They are not surrounded by concentric
lamellae of bone.
 Also known as perforating canal
VOLKMANN’S CANAL

12. Consists of poorly organized trabeculae
(small needle-like pieces of bone)
Lot of open space between them.
Nourished by diffusion from nearby
Haversian canals.
MICROSCOPIC STRUCTURE OF SPONGY
(CANCELLEOUS) BONE

13. COMPOSITION OF BONE

15. Also known as bone gamma-carboxyglutamic acid-containing protein
(BGLAP), is a noncollagenous protein found in bone and dentin.
Its synthesis is vitamin K dependent.
 Secreted solely by osteoblasts
 In bone mineralization and calcium ion homeostasis.
OSTEOCALCIN

16. It is a glycoprotein in the bone that binds calcium. It is secreted by osteoblasts during bone
formation, initiating mineralization and promoting mineral crystal formation.
 Osteonectin also increases the production and activity of matrix metalloproteinases, a
function important to invading cancer cells within bone.
OSTEONECTIN
OSTEOPONTIN
 also known as bone sialoprotein I (BSP-1 or BNSP)
 plays role in mineralization and bone remodelling.

17. Alveolar bone is defined as the parts of maxilla and mandible that form
and support the socket of teeth.
(CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY)- Jan Lindhe pg:34
Together with the root cementum and periodontal ligament, the alveolar
bone constitutes the attachment apparatus of the teeth.
Forms when tooth erupts to provide osseous attachment to the forming
PDL, disappears gradually after tooth is lost.

18. Develops and undergo remodeling with tooth formation, hence tooth-dependent
bony structures.
Size, shape, location and function of teeth determine their morphology.

19. Alveolar process consists of bone which is formed both by cells from the dental follicle
(alveolar bone proper) & cells which are independent of tooth development.
Maxilla & mandible develop-- 1st branchial arch or mandibular arch.
The maxilla forms within the maxillary process & mandible forms within the fused
mandibular processes of mandibular arch.
Both jaw bones start as small centers of intramembranous ossification around stomodeum.

20. 8th week in utero.
Alveolar process develops from dental follicle
during eruption of teeth.
Bell stage developing bone becomes closely
related.
Teeth separated from each other by the
development of interdental septa.

21. The developing teeth lie in a trough of bone –tooth
Crypt.
Resorption – inner wall of the alveolus
Deposition –outer wall
The size of the alveolus is dependent upon the
size of the growing tooth germ.

22. With the onset of root formation, interradicular
bone develops in multirooted teeth.
When a deciduous tooth is shed, its alveolar
bone is resorbed.
Alveolar process gradually incorporated into
maxillary or mandibular body.
Permanent tooth moves into place, developing
its own alveolar bone from its own follicle.

24. Osteoblast synthesize and lay
down precursors of type 1
collagen
They also produce osteocalcin
and the proteoglycans of
ground substance & rich in ALP
Collagen formed by osteoblast
is deposited in parallel or
concentric layers to produce
mature bone
When bone is rapidly formed as in certain
conditions(fracture callus), the collagen is
not deposited in a parallel array but in a
basket like weave and is called woven,
immature or primitive bone.
The main mineral component
of bone is an imperfectly
crystalline hydroxyapatite. The
mineral crystals are deposited
along and in close relation to
the bone collagen fibrils.
Calcium and phosphorous are
derived from the blood plasma
and from nutritional sources.
The extracellular matrix of
bone is mineralized soon after
its deposition
Very thin layer of
unmineralized matrix is seen
on the bone surface and this is
called the osteoid layer or
osteoid seam.
As the process of bone
formation progresses the
osteoblast come to lie in tiny
spaces within the surrounding
mineralized matrix and are
then called osteocytes.

26. MAXILLA
&
MANDIBLE
ALVEOLAR
PROCESS
ALVEOLAR BONE PROPER
SUPPORTING ALVEOLAR
BONE
BASAL BONE
CORTICAL PLATES
BUCCAL AND LINGUAL
SPONGY
BONE

27. Alveolar bone proper is the bone forming the tooth socket or the alveolus that
surrounds the root of the tooth.
Histologically it is a compact bone having osteons.
It is also called bundle bone since bundles of principle periodontal ligaments fibres
called sharpey’s fibres attach to the bone from the tooth.
It has numerous small perforations of canals that carry blood vessels and nerves and
blood vessels.
Its also called the cribriform plate.

28. Radiographically it can be seen as a thin radio-
opaque bone surrounding the roots of teeth
and is called lamina dura.
Break in continuity of lamina dura at the
proximal aspects of crest of interdental septum
has been considered as the earliest
radiographic change in periodontitis.
Its divided into two parts- Lamellated &
Bundle Bone

29. It is that part of the bone which surrounds the
alveolar bone proper and gives supports to the
socket.
It consists of two parts : a. Cortical plates
b. Spongy bone :

32. Formed when the inner and outer cortical
plates meet
The margin is thin & knife edged in vestibular
surfaces of anterior and rounded/beaded in
posterior teeth
 Most prominent border of interdental septum
INTERRADICULAR SEPTA
 The bone between the roots of multirooted
teeth .
 Both of them contain perforating canals of
Zukerkandl & Hirschfeld [nutrient canals].

34. CELLS
OSTEOGENNIC
CELLS
OSTEOCLASTIC CELLS
OSTEOBLASTS
OSTEOCYTES
BONE LINING
CELLS
OSTEOPROGENITOR
CELLS
OSTEOCLASTS

40. Cathepsin-K
I. It is a collagenolytic enzyme.
II. Degrades major amount of Type I Collagen and other
noncollagenous proteins
Matrix metalloproteinase
(MMPs)
I. MMP-9 (Collagenase B) – osteoclast migration.
II. MMP-13- osteoclast differentiation.
ENZYMES OF OSTEOCLAST

43. Tartarate resistant acid phosphatase (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, the lysosomes,
the Golgi cisternae and vesicles.
INTRACELLULAR ROLE OF TRAP
Intracellularly TRAP has been localized in the vesicles of osteoclasts.
It is released into the extracellular environment as an active enzyme by exocytosis.
ROLE OF TRAP IN BONE RESORPTION

45. VASCULAR SUPPLY

48. PLATELET DERIVED GROWTH FACTOR
Increases
bone
collagen
synthesis
and rate of
bone
matrix
apposition.
Produced
by
osteoblasts.
Mainly
derived
from serum
and
platelets.
Stimulates
DNA
synthesis
and cell
replication
in
osteoblasts.

49. Synthesized by osteoblasts in an active form
Stimulate
1. preosteoblastic cell replication
2. Osteoblastic collagen synthesis
3. Bone matrix apposition
4. Alkaline phosphatase activity
FIBROBLASTS GROWTH FACTOR
Exerts its effects on bone formation ,primarily through increased
proliferation of osteoprogenitor cells
Promotion of osteogenic differentiation
TRANSFORMING GROWTH FACTOR Β

50. BONE MORPHOGENIC PROTEINS
Belonging to TGF- β(transforming growth factor beta ) family ,possessing
osteo inductive qualities
Induces
I. Chondrocyte differentiation
II. Matrix mineralization
III. Osteoblasts precursor cells into more mature osteoblasts
IV. Collagen production by mature osteoblasts

51. PARATHORMONE
PTH affects
bone cell
function, may
alter bone
remodeling, and
cause bone loss.
PTH acts on
both bone
resorbing cells
(osteoclasts)
and bone
forming cells
(osteoblasts)
It increases
osteoclastic
bone resorption
and supresses
bone formation
if administered
continuously.
When
administered in
low doses
intermittently it
stimulates bone
formation.
(Anabolic
effect)

52. VITAMIN D3
Stimulates
osteoclastic
bone
resorption in
vitro and in
vivo & has very
slow onset of
action.
Increases
osteoclast no.
and activity
along with
ruffled border
size and clear
zone volume.
It has a shallow
dose response
curve.

53. CALCITONIN
Inhibit
Osteoclastic Bone
Resorption
Effects are short
lived and there is
decreased
sensitivity after
prolonged
exposure.
It occurs due to
decrease in
receptors and
second population
of osteoclasts that
are non
responsive to
calcitonin.

54. MEDIATORS OF BONE RESORPTION

55. BONE MULTICELLULAR UNIT
Bone remodeling are characterized by the presence of a BMU
(bone multicellular units) .
1. Osteoclasts
2. Osteoblasts
3. Blood vessels & Pericytes
Each unit is organized into "cutting cone" of osteoclasts
reabsorbing bone followed by trail of osteoblasts reforming
the bone to fill defect

60. The main functions of remodeling are-
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.
Regulation of bone remodeling is a complex process involving hormones and
local factors acting in a autocrine and paracrine manner on the generation and
activity of differentiated bone cells – Sodek et al 2000

61. •Functional requirements
•Age related changes in
bone cells
LOCAL
INFLUENCES
•Hormones (PTH)
•Vitamin D, Calcitonin
SYSTEMIC
INFLUENCES
FACTORS INFLUENCING REMODELLING

62. BONE RESORBERS BONE PROTECTORS
Parathyroid hormone, vitamin D3 calcitonin
Cytokines , IL -1, IL-6 Bisphosphonates , statins
TNF alpha & beta Osteoprotegerin
Colony stimulating factors Interferon gamma
Prostaglandins & Arachidonic acid metabolites Glucocorticoids , Indomethacin/ Aspirin
RANKL/ OPG-L IL-1 receptors antagonist
Bacterial products Estrogen & leptin
MEDIATORS IN BONE REMODELLING

63. Conditions involving loss of alveolar bone:
Extension of gingival inflammation
 Trauma from occlusion
Systemic factors
Periodontitis
ALVEOLAR BONE IN DISEASE

64. • Most common cause of bone loss in
periodontal disease is extension of
inflammation from marginal gingiva into
supporting periodontal tissues.
• Spread of inflammation from gingiva
directly to PDL is less frequent.
• The transition from gingivitis to
periodontitis is associated with changes in
composition of bacterial plaque.
• In advanced stages number of motile
organisms and spirochetes increases.
BONE DISTRUCTION CAUSED BY EXTENTION OF
GINGIVAL INFLAMMATION :

65.  Vit-D deficiency
 Diabetes Mellitus
 Hyperparathyroidism
 Leukaemia
 Fibrous dysplasia
 Osteomyelitis
Bone Destruction by Systemic Disease

66. Vitamin D or calciferol - absorption of calcium from the GIT
 Experimental studies showed that in osteomalacia, there is rapid, generalized severe
osteoclastic resorption of alveolar bone, proliferation of fibroblasts that replace bone and
marrow, and new bone formation around the remnants of un resorbed bony trabeculae.
 Radiologically there is generalized partial to complete loss of lamina dura and reduced
density of supporting bone, loss of trabeculae. Increased radiolucency of trabecular
interstices and increased prominence of remaining trabeculae.
VITAMIN D DEFICIENCY

67.  Hyperglycemia induces - production of macrophage colony stimulating factor
(M-CSF), Tumor Necrosis Factor –α and RANKL, all of which are osteoblast derived
activators of osteoclast proliferation and differentiation.
 Further suppression of osteoblast proliferation takes place by decreasing
osteocalcin and osteopontin expressions.
Bone quality is also reduced as a result of :
1. Polymorphonuclear Leukocyte Function.
2. Collagen Metabolism and Advanced Glycation End products.
ALVEOLAR BONE LOSS PROGRESSION IN DIABETES MELLITUS

68. AUTHOR &
JOURNAL
TITLE RESULT CONCLUSION LEVEL
OF
EVIDENCE
TELLERVO TERVONEN
et. al.
JOURNAL OF CLINICAL
PERIODONTOLOGY
Alveolar Bone
Loss in type 1
Diabetic Subjects
Type 1 DM has a
modifying effect on
marginal loss of alveolar
bone. A clear trend
towards increased
marginal bone loss was
seen in the subjects with
complicated DM The
subjects with good
metabolic control and no
complications of DM are
no more susceptible to
marginal bone loss than
non‐diabetic controls of
the same age.
The present
findings confirm
our previous
results on
increased loss of
periodontal
support in subjects
with complicated
DM already at an
early age.
1B

69.  Oral changes include malocclusion and tooth mobility, radiographic evidence of
alveolar osteoporosis with closely meshed trabeculae, widening of the lamina dura, and
radiolucent cyst like spaces.
 Bone cysts become filled with fibrous tissue with abundant hemosiderin- laden
macrophages and giant cells. They have been called brown tumors, although they are
not really tumors but reparative giant cell granulomas.
 This disease is called osteitis fibrosa cystica or Von Recklinghausen’s disease.
 Other diseases in which it may occur are Paget’s disease, fibrous dysplasia, and
osteomalacia.
HYPERPARATHYROIDISM

72. The relationship between endosseous implants and bone consists of one of the two mechanism:
1) Osseointegration: when the bone is in intimate but not ultrastructural contact with
implant. Osseointegration concept proposed by Branemark et al
2) Fibrosseous integration, in which soft tissues such as fibers and/or cells, are interposed
between the two surfaces.
BONE IMPLANT INTERFACE
OSSEOINTEGRATION FIBROSSEOUS INTEGRATION

73.  Incorporation of woven bone
 Adaptation of bone mass to load (lamellar
bone deposition)
 Adaptation of bone structure to load (bone
remodelling)
STEPS OF OSSEOINTEGRATION

74. BONE DENSITY FOR IMPLANTS