By S.

Gnana Sekar

Post Graduate Student

Dept. of Periodontics ,
GDC,VIJAYAWADA.
CONTENTS :
WHAT IS A BONE ?

COMPOSITION OF BONE .

IS THERE ANY DIFFERENCE BETWEEN ALVEOLAR BONE AND NORMAL

BONE ?

DEVELOPMENT OF ALVEOLAR PROCESS

STRUCTURE OF ALVEOLAR PROCESS

NERVE SUPPLY OF ALVEOLAR BONE

BLOOD SUPPLLY OF ALVEOLAR BONE

LYMPHATIC DRAINAGE OF ALVEOLAR BONE

ALVEOLAR BONE; RADIOGRAPHIC INTERORETATION

AGE CHANGES IN ALVEOLAR PROCESS

 HISTOLOGY OF ALVEOLAR BONE

 REMODELLING OF BONE

 FACTORS REGULATING BONE FORMATION

 FACTORS REGULATING BONE RESORPTION

 REGULATION OF BONE BY SYSTEMIC HORMONES

 BONE COUPLING

 ALVEOLAR BONE IN DISEASE

 (a)Bone destruction caused by extension of gingival inflammation

 (b) Pharmacologic Agents & Bone Resorption

 (c)Bone destruction caused by trauma of occlusion

 BONE REGERATIVE PROCEDURES

 REFERENCES
 WHAT IS A BONE ?????
COMPOSITION : Inorganic material – 65%
Hydroxyapatite
Organic material – 35%
Collagen (Type – I) 88% - 89%
Noncollagen 11% - 12%
- Glycoproteins 6.5% - 10%
- Proteoglycans 0.8%
- Sialoproteins - 0.35%

- Lipids - 0.4%

Only a subset of BMPs, most

notably BMP 2,4,6,7,9 has
osteoinductive activity.
Osteocalcin - also known as bone gamma-carboxyglutamic acid-containing protein (BGLAP),
is a noncollagenous protein found in bone and dentin.
 Because it has gla domains, its synthesis is vitamin K dependent.
 Osteocalcin is secreted solely by osteoblasts
 In bone mineralization and calcium ion homeostasis.

Osteonectin - 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.

Osteopontin (OPN) - also known as bone sialoprotein I (BSP-1 or BNSP) –plays role in
mineralization and bone remodelling.
What is alveolar bone ???

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.

Develops and undergo remodeling with tooth

formation, hence tooth-dependent bony structures.

Size, shape, location and function of teeth determine

their morphology.
IS THERE ANY DIFFERENCE BETWEEN NORMAL
BONE AND ALVEOLAR PROCESS /BONE ????
DEVELOPMENT OF ALVEOLAR PROCESS………
DEVELOPMENT OF ALVEOLAR
PROCESS .

Meckel’s cartilage
For its development & maintenance

 
Morphology of Alv. Bone depends on
Size
Shape
                                                                                                  
position of teeth

If teeth are lost, Alv bone undergoes atrophy

If teeth congenitally missing – Alv. Bone not developed
 STRUCTURE OF ALVEOLAR PROCESS :
The alveolar process is composed of
two parts. They are

(1)Alveolar bone proper

(2)Supporting alveolar bone
 Jaw bones

Alveolar
Basal bone
process
Supporting
Cortical plates
alveolar
buccal ,lingual
Alveolar bone
bone proper Spongy bone
1 Alveolar bone proper :
It consists of a thin lamella of bone that A
surrounds the root of the tooth and give B
attachment to principle fibers of the
periodontal ligament. C
Anatomically called as –
Histologically called as –
Radiologically called as -

- It is perforated by many openings Histologic section

that carry nerves and blood vessels in to showing foramen in
the periodontal ligament therefore it is alveolar bone proper
called cribriform plate. (cribriformligament
A-Periodontal plate)
- B-Cementum
C-Foramen in alv. Bone proper
- Consist of lamellated bone and
bundle bone.

The bundle bone is that bone in which

the principal fibers of the periodontal
ligament are anchored.

The term “bundle bone” was chosen

because the bundles of the principal
fibers continue in to bone as sharpey’s
fibers.

Bundle bone
2.supporting alveolar bone :

: 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 :
a.    CORTICAL  PLATES  :  (1.5-3mm  thick  in 
posterior  tooth  region  and  thickness  varies  in 
anterior region )
- It consists of compact bone and form the outer
and inner plates of the alveolar processes.

- It is continuous with the bony maxilla and

mandible and is much thicker in the mandible than
in the maxilla. They are thickest in the mandibular
premolar and molar regions especially on the buccal
side.
- In the maxilla the outer cortical plate is
perforated by many small openings through which
blood and lymph vessels pass. In the mandible it is
dense.
b.   SPONGY BONE :

- It fills the area between cortical plates and the alveolar

bone proper.

- In the region of the anterior teeth of both jaws the

supporting bone is usually thin, so no spongy bone is found
here.
Roentgenographic features
-      Roentgenograms  permits  the 
classification of the  spongiosa of  the 
alveolar process in to two main types.

Type  :  I  :-  interdental  and 

interradicular  trabecular  are  regular 
and  horizontal  in  a  ladder  like 
arrangement.
Type-I
More  common in mandible.
 

Type  :  II :-  shows irregularly 
arranged, numerous delicate 
interdental and interradicular 
trabecular.

Type-II  More common in maxilla. 
Histology of Alveolar bone :

Figure shows Haversian system
The interdental and interradicular
septa contain the perforating canals
of Zuckerkandl and Hirschfeld
(Nutrient canals),which house the
interdental and interradicular
arteries ,veins ,lymph vessels and
nerves.
Tooth

Nutrient canal
          CREST OF ALVEOLAR BONE :
The shape of the outlines of the crest of the alveolar septa in the 
roentgenogram is dependent on the position of the adjacent teeth. 
In
lth
         H ea

1.5-2mm  –  always  maintained  through  out  the  life  and  is           

constant.

Diagram of relation between CE junction of 
adjacent teeth shape of crest of alveolar septa
Nerve Supply of Alveolar Bone
Blood Supply of Alveolar Bone
Lymphatic Drainage of Alveolar Bone
Osteoprogenitor cells :
Undifferentiated mesenchymal cells and
hemotopoetic stem cells – under certain
circumstances they divide and transform in to
osteoblasts and osteoclasts.

y
 RUNX2 is a key transcription factor associated with osteoblast differentiation.

β-catenin is a subunit of the cadherin protein complex 
and acts as an intracellular signal transducer
 in the Wnt signaling pathway.

colony stimulating factor 1 (CSF1), also known as macrophage colony-stimulating factor (M-CSF), is a
secreted cytokine which influences hematopoietic stem cells to differentiate into macrophages or other related cell types
 RANKL
Member of the tumor necrosis factor (TNF) cytokine family.
Also known as –
 Tumor necrosis factor ligand superfamily member 11 (TNFSF11),
 TNF-related activation-induced cytokine (TRANCE),
 osteoprotegerin ligand (OPGL), and
 osteoclast differentiation factor (ODF)

 Bone marrow expresses low levels of RANKL, it plays a critical role for adequate bone metabolism,
this surface-bound molecule (also known as CD254) found on osteoblasts serves to activate
osteoclasts, which are critically involved in bone resorption.

 Osteoclastic activity is triggered via the osteoblasts' surface-bound RANKL activating the osteoclasts'
surface-bound receptor activator of nuclear factor kappa-B (RANK).

 stimulation of osteoclast diffrentiation and bone resorption (lacey et.al 1998 ,kong et al 1999 )

 Anti-RANKL antibody - Denosumab

 RANK
 Member of the tumor necrosis factor receptor (TNFR) cytokine
family

 Also known as TRANCE Receptor or TNFRSF11A

 RANK is the receptor for RANK-Ligand (RANKL) and part of the RANK/RANKL/OPG
signaling pathway that regulates osteoclast differentiation and activation

 RANKL binds to RANK, which then binds to TRAF6

TRAF6 stimulates the activation of the c-jun N-terminal kinase (JNK) and nuclear
factor kappa-b (NF-kB) pathways

which trigger differentiation and activation of osteoclasts.

OSTEOPROTEGERIN
 Osteoprotegerin is a cytokine receptor, and a member of the tumor necrosis
factor (TNF) receptor superfamily.

 Also known as osteoclastogenesis inhibitory factor (OCIF), or tumor

necrosis factor receptor superfamily member 11B (TNFRSF11B).

 Acts as a decoy and blocks the binding of RANKL to RANK and thus prevents
Osteoclastogenesis
 OSTEOGENIC LINE OF CELLS :
Osteoblasts :

Derived  from…….  multipotent  UNDIFFERENTIATED 

mesenchymal  cells  or  alternatively  from  perivascular  cells 
(PERICYTES).

Secretes  both    “collagenous(type  1  collagen)  and  non  collagenous” 

bone matrix – OSTEOID .         

Osteoblasts  exhibit  high  level  of  alkaline  phosphatase  on  their  outer 
plasma  membrane  -    believed  to  contribute  -    initiation  of  bone 
mineralization. BMP 2,7 -osteoinductive
PDG-F
During osteogenesis osteoblasts secrete GF  
IGF’S
  TGF-β
 FUNCTIONS :

 Regulation of osteoclasts and deposition of bone matrix ( MACKIE 2003)

 Bone remodeling and mineral metabolism

 Mineralization of new bone

 Secrete type I collagen ,type V collagen, osteonectin, osteopontin ,RANKL,

osteoprotegerin, growth factors

 Osteocalcin and CBFA1

 Express alkaline phosphatase

 Recognize resorptive signal and transmit to osteoclast.

 CBFA-1 – regulate the expression of osteoprotegerin.

 OSTEOCYTES : (NERVE CELLS OF BONE )
Most abundant bone cells .

Communicate with each other and with other cells on surface 
of the bone via dendritic process encapsulated in canaliculi

Play role in calcium homeostasis

Exchange of metabolic and 
biochemical messages occurs
 between blood stream and canaliculi  

 Acts as  mechanosensors instructing osteoclasts where 
to resorb and osteoblasts where and 
when to form (BOULPAEP AND BORON 2005 : 
MANOLAGAS 2000 )
Osteoclasts : (2-10 or as many as 50 nuclei)

Generally occur in clusters.     
 
They have prominent mitochondria, 
lysozomes, vacuoles and 
few endoplasmic reticulum.

Activity is controlled by PTH

They are found against the 
bone surface, occupying shallow
 depressions called Howship’s lacunae
surfaces or in deep resorption cavities
 called cutting cones.

Sequence of events;
 Removal of mineral/inorganic Matrix
 Degradation of org. matrix
Morphologic Characteristics
Ruffled/ Striated border
Clear zone
MORPHOLOGY :
   40 to 100 microns in diameter
   15 to 20 closely packed nuclei
   Variable in shape
BONE LINING CELLS :

Similar to osteocytes – i.e., osteoblasts that do not get embedded
 in newly formed bone ,gets adhered to the outer surface of the bone

…..when bone formation halts.  
Bone modeling and remodelling ….( does both
same???)
    In  the  haversian  canals,  closest  to  the  surface, 
osteoclasts  differentiate  and  resorb  the  haversian 
lamellae and part of circumferential lamellae which is 
replaced  by  proliferating  loose  connective  tissue. 
This  area  of  resorption  is  called  the  cutting  cone  or 
the resorption tunnel.

Light micrograph of bone turnover. A, Cutting cone in cross section. 
Large multinucleated osteoclasts resorb an old osteon. B, Filling cone in 
cross section. Uninucleated osteoblasts ring the partially formed osteon .
 Bone remodeling
REMODELING  involves  the removal of discrete packets of  old bone ,replacement of 
these packets with newly synthesised protenaceous matrix and subsequent 
mineralization of the matrixto form new bone . ( fernandez –tresguerres –hernandez 
et.al 2006 )
 Remodeling of bone
Bone multicellular unit(BMU):
local groups of osteoblasts and osteoclasts involved in bone remodelling is called bone multicellular
units (BMU).
- each unit is organized into "cutting cone" of osteoclasts reabsorbing bone followed by trail of
osteoblasts reforming the bone to fill defect

Osteoclast recruitment
Resorption
Osteoblast recruitment
Origination
Osteiod formation
Mineralization
Mineral maturation
Quiescence:
osteoblasts become resting bone lining cells on the newly formed bone surface
 If OPG+RANKL=inhibit osteoclast genesis
Osteoblast OPG

RANKL

RANK
RANK

RANKL
+RANK
Osteoclast progenitor cell
Mature osteoclast

RANKL+RAaNK

Bone resorption
 BONE COUPLING:

New bone formation occurs at bone resorption sites in each cycle of bone remodeling to maintain the microarchitecture required for bone's 
mechanical properties. This is achieved through different levels of cellular communication. In bone matrix, TGF-β1, and probably IGF-1, act as 
the primary coupling factors and are released in response to osteoclastic bone resorption. These factors induce the migration of osteoblastic cells so 
that the new bone formation is spatiotemporally coupled with resorption through this mode of matricellular signaling. Negishi-Koga et al now 
reveal that Sema4D secreted from osteoclasts regulates osteoblast differentiation; Sema4D activates downstream of RhoA by binding to Plexin-B. 
RhoA also mediates the actions of both TGF-β1 and IGF-1. Thus, the matricellular signaling of TGF-β1 and IGF-1 is integrated with Sema4D–
Plexin-B1–mediated osteoclast-osteoblast communication through RhoA. RANK-RANKL mediates communication to induce differentiation of 
osteoclast progenitors. Osteoclastic production of Sema4D is stimulated by increased osteoblastic RANKL. Sema4D then inhibits osteoblast 
differentiation to balance the supply of osteoclasts and osteoblasts, thus functioning in a negative-feedback loop.
Factors regulating Bone Formation
1. Platlet derived growth factor
2. Heparin binding growth factor
3. Insulin like growth factor
4. Transforming growth factor
5. Bone morphogenic protein
Factors regulating Bone Resorption
1. IL 1
2. IL 6
3. TNF & Lymphotoxins
4. Gamma interferon
5. Colony stimulating factors
6. Prostaglandin & other Arachidonic Acid metabolites
Regulation of Bone by systemic hormones
1. Parathyroid hormone
2. 1,25 Dihydroxy vit D3
3. Calcitonin
4. Estrogen
 AT MICROSCOPIC LEVEL :
4 types of bones are seen ….

Plays main role
 in healing  Composite
Phase I bone/
Woven bone  bone
It forms very quickly       
(30-60mm/day) 
And resorbs very quickly

Phase II bone/
lamellar bone/
Mature load Bundle bone
Forms very slowly
 (0.6-1mm/day)
 bearing bone
 AGE CHANGES :

Changes in the alveolar bone with aging are similar to

those occurring in the reminder of the skeletal
system.
More irregular periodontal surface of bone
Less regular insertion of collagen fibers
Osteoporosis
Decreased vascularity.
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

I. Periodontitis
II. Periodontal abscess
III. Food impaction
IV. Overhanging restoration
V. Adjacent tooth extraction
VI. Ill-fitting prosthesis
BONE DISTRUCTION 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.
Spread of inflammation from gingiva directly to PDL
is less frequent.

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.
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.

Rate of bone loss

 In study of Srilankan labourers with no oral hygiene & no dental

care Loe & associates found the rate of bone loss to average
about 0.2mm a year for facial surfaces & about 0.3mm a year for
proximal surfaces.
Bone Destruction Pattern in Periodontal Disease

Horizontal bone loss
 Most common pattern of bone loss in periodontal
disease.
 Bone is reduced in height but margin remain almost
perpendicular to tooth surface not necessarily equal
degree around same tooth

Bone deformities
 Careful probing & surgical exposure required to
determine exact dimension of the defect
 Vertical / Angular bone defect
.
These defects are classified on bases of No. of osseous walls
present :  
walls remain intact.
Three wall
defect Combined defect

Two wall
defect

No.of walls in the apical portion of the 
defect is greater than its 
One wall occlusal portion .
defect
Crater:
Concavities in the crest 
of interdental bone

Most common osseous 
Defect -35.2 %

Most common in
Mandible – 62%
Bulbous bone contour (Exostosis) :

Bony enlargements caused by 
adaptation to function or
 buttressing bone formation
 etc.

More frequently found in 
maxilla.
Reverse Architecture

Caused because of loss of interdental, facial&/lingual

wall without concomitant loss of radicular bone

-Maxilla
 Ledges :
Plateau like bone margins caused by resorption of
thickened bony plates .
Bone Destruction caused by Trauma from
Occlusion
 Def:” when occlusal forces exceeds the adaptive capacity of the tissue , tissue
injury results k/a Trauma from occlusion

 Primary trauma from occlusion:

Alteration in occlusal forces in Normal
periodontioum with normal height of bone

 Secondary trauma from occlusion :

Due to reduced ability of tissues to resist forces;
in cases of :Normal periodontium with reduced
height of bone &Marginal periodontitis with
reduced height of bone
 Studies related to TFO

Miyata T,Kobayashi Y, Araki H, et al;The influence of

controlled occlusal overload on periimplant tissue; A
histologic study in monkey ;2000.

Isidor F; Loss of ossiointegraion by occlusal load of oral

implants;A clinical & radiographic study in monkeys;1996.

Harrel SK ,Nunn ME, The effect of occlusal discrepancies

on peridontitis; 2001.
Bone Destruction by Systemic Disease
 Vit-D deficiency
 Diabetes
 Hyperparathyroidism
 Leukemia
 Paget’s disease
 Fibous dysplasia
 Histiocytosis ,X ,
 Osteomyelitis
 Central giant cell granuloma
 Aneurysmal bone cyst
 Vitamin D deficiency:

 Vitamin D or calciferol - absorption of calcium from the gastrointestinal tract and the
maintenance of the calcium phosphorous balance.

 Experimental studies in animals 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 unresorbed bony
trabeculae.
 Radiologically there is generalized partial to complete loss of lamina dura and reduced
density of supporting bone, loss of trabeculae. Increased radiolucence of trabecular
interstices and increased prominence of remaining trabeculae.
BOTH DEFICIENCY AND
EXCESS…..????
 Vitamin D at normal physiologic levels act on intestinal mucosa and the renal distal
tubule to increase the absorption of Calcium. This Calcium will then be available for use
in mineralizing new bone formation.

 Therefore, when you have Vitamin D deficiency you will develop rickets (in children) or
osteopenia (in adults).

 The issue, is that if you have too much of Vitamin D (Vitamin D excess) then at that
time it will work on the nuclear receptors in the osteoblasts and promote bone
resorption. – they bind to vitd receptor on osteoblasts and stimuates the
expression of RANK-L - which in turn induces osteoclastogenesis

 Therefore, both deficiency and excess of Vitamin D can cause osteopenia and bone
resorption.

- From kaplans Textbook of physiology

Alveolar Bone Loss Progression
in Diabetes:

 Taylor et al suggested that poorer glycemic control leads to both an increased risk for
alveolar bone loss and more severe progression.

 Factors potentially contributing to development of periodontal disease

as per the Position Paper on Diabetes and Periodontal Diseases published in the August
1999.
 1. Polymorphonuclear Leukocyte Function.
 2. Collagen Metabolism and Advanced Glycation End products.
HYPERGLYCEMIA –ACTIVATES
OSTEOCLASTS …BUT
HOW?????
 Hyperglycemia induces - production of macrophage colony stimulating factor(M-CSF),
Tumor Necrosis Factor –α and Rank L, 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 advanced glycation end products, which
eventually results in fractures.
 Hyperparathyroidism :
 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.
 Hematological disorders:

 In leukemia , the presence of infiltrate in marrow spaces and the periodontal ligament
results in osteoporosis of alveolar bone with destruction of the supporting bone and
disappearance of periodontal fibers. (the malignant T-lymphocytes produced an osteoclast-activating-factor-like
substance that caused osteoclast proliferation and hypercalcemia.)

 In Sickle cell anemia generalized osteoporosis of the jaws, with a peculiar stepladder
alignment of the trabeculae of interdental septa and pallor and yellowish discoloration of
oral mucosa.
Pagets disease :
In pagets disease - Osteoclasts and osteoclast
precursors contain paramyxoviral transcripts and
appear hyperresponsive to 1,25-(OH)2D3 and
RANK ligand (RANKL).
Osteoclasts in Paget's disease are increased both in
number and size
BONE REGENERATION :
 Osteogenesis is the ability of the graft to produce new bone, and this process is dependent on
the presence of live bone cells in the graft.

 Osteoconduction is the physical property of the graft to serve as a scaffold for viable bone
healing. Osteoconduction allows for the ingrowth of neovasculature and the infiltration of
osteogenic precursor cells into the graft site.

 Osteoinduction is the ability of graft material to induce stem cells to differentiate into mature
bone cells. This process is typically associated with the presence of bone growth factors within the
graft material or as a supplement to the bone graft.
BONE GRAFTS :
Is there any relation between bisphosponates
and
osteoradionecrosis of jaw ??????
References:

Orban’s oral Histology &Embryology.

Fundaments of periodontics second edition by Thomos G.

wilson’jr DDS ;Knneth S. Kornman’DDS,pHd

Clinical periodontology 12th edition by Neeman

,Takei,carranza

Journal of clinical periodontology Vol;27jan-May-2000;j-

272

the dental clinics of North America;Advances in

periodontics part -1 by david C. vandersall Vol-42,No.2,
Apr.1998
Contemporary Periodontics by Robert J. Jenco; Henry
M>.Goldman ;D.Walter Cohen

Clinical Dentistry in Health & Dease,vol-2 The Mouth &

Perioral tissue Crispian scully

Periodontal Diseae Clinical ,Radiologic, Histopathologic

features by Glickman –pSumlow

di Fiore’ s atlas of Hitology

 Guided by

Dr.Narendra dev
(HOD &Prof)
Dr.S.V.Madhuri
(ASSO. Prof)
Presented by Dr.B.Lahari
Dr.s.Gnana sekar, (ASSIS.Prof)
GDC ,VJD.