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Questions

Diameter of microcytesTotal no of collagen fibers identifiedAnchoring fibersOxygen consumption of gingivaTime taken for the formation of LJEProliferation and differentiation of gingivaGingival bleeding

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P R E S E N T E D B Y

D R . S H E E M A

1 S T Y E A R P G

Alveolar bone in health and diseases

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Contents

Introduction and development Molecular biology of

developmentAlveolar boneStructure and composition Cells MatrixRemodelingResorption OsteoimmunologyBone destruction caused by

gingival inflammationRadius of action

Lipopolysaccharides mediated bone destruction

Effect of Prostaglandins on boneTrauma from occlusion Bone in periodontitisBone loss patternsTherapeutic approaches to treat

pathological bone lossBone graft materialsGuided bone regenerationConclusion References

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Introduction and development

Endochondral ossification

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Intramembranous ossification

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Sutural bone formation

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Molecular biology

TGF-β

Reddi et.al – BMPS

Differentiation

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Alveolar bone

“ Alveolar process is defined as the part of the maxilla and

mandible that form and support the tooth socket”

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Structure of the alveolar bone

Alveolar bone proper

Supporting alveolar bone

Cortical plates

Spongy bone

Interdental septum

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Periosteum and endosteum

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Fenestration and Dehiscences

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Composition

Osteoblasts

Osteocytes

Osteoclasts

Matrix components

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Osteoblasts

Mesenchymal origin – Scherft JP, Groot CG 1990

Organic matrix – type I collegen

Actin, myosin and cytoskeleton proteins

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Formation

Pluripotent stromal cells – Inducible osteoprogentior cells

(IOPC’s)

BMP’s + growth factors – determined osteoprogenitor cells

(DOPC’s)

Mature osteoblasts

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Function

Bone formation

Type I and V collagen

Ground substances

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Stimulus of various substances

Parathyroid hormone

Vitamin D3

Growth hormones

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Osteocytes

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Osteoclasts

Greek word – bone and brokeHowship’s lacunae

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Formation

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Matrix

Organic matrix -35% of dry weight

Inorganic matrix - 60-70% of dry weight

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Matrix

Collagen :

Type I > 95%

Type V 5 %

Type III and type XII – (Lukinmaa 1992)

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Non collagenous proteins

Osteocalcin:

Also know as bone gla protein

Regulates mineral maturation of bone

Calcium binding protein

Regulated by Vit D3 and PTH

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Osteopontin and bone sailoprotein

BSP – mineralizing tissues

Osteopontin – generalized distribution

Vit D3 – up regulates Osteopontin, suppress BSP

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Osteonectin / SPARC

25%

Calcium binding glycoprotein

Regulates cell adhesion

Proliferation & modulation of cytokines

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Proteoglycans

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Bone Remodeling

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Factors effecting Remodeling

PTH

Calciton

Vit D3

Cytokines

Platelet – derived growth factor

IGF

FGF

Androgen

Estrogen

Progesterone

Insulin

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Bone resorption

Tencates 1994 – sequence of events in resorption process

IL-I

IL-6

TNF α

CSF

Prostaglandins

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Stimulators Inhibitors

IL 1

IL 6

TNF α

PTH

Vit D3

M-CSF

RANK

RANKL

OPG

Estrogen

Androgen

Calciton

INF gamma

Mediators and inhibitors of bone resorption

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Alveolar bone in diseases

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Osteoimmunology

Relation between immune system and bone metabolism –

osteoimmunology

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Macrophage colony stimulating factor

M-CSF – Osteoclasts development and activation

Produced – Osteoblasts

Osteoclstogenesis

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RANK and RANKL

RANK- Receptor Activator for Nuclear factor Kappa B

RANKL - Receptor Activator for Nuclear factor Kappa B Ligand

RANK + RANKL = osteoclasts formation

RANKL upregulated by TNF α and IL-1 (Lopes.J 2009)

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RANK and RANKL

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RANK and RANKL

Elevated expression in inflamed periodontal tissue – Cochran DL 2008

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Osteoprotegerin (OPG)

Natural inhibitor of RANKL

Blocks RANK + RANKL

OPG produced by PDL cells, gingival fibroblasts and epithelial

cells (Kanzaki 2002)

Reduced OPG adjunct to granulation tissue (Crotti 2003)

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RANKL and OPG ratio

Increased ratio in inflamed tissues

Increased RANKL

Decreased OPG

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Bone destruction caused by gingival inflammation

Gingival inflammation extends along the collagen fiber bundles

and follow the course of the blood vessels through the loosely

arranged tissue around them into the alveolar bone – Hansen ER

1966

Bone destruction in periodontal disease is not a process of bone

necrosis – Kronfeld 1935

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Path of inflammation

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Radius of action

Garant and Cho 1979 –factor may need to present closely

Page and Schroder 1982 – 1.5-2.5mm

Large defects greatly exceeding 2.5 mm from tooth – presences

of bacteria in tissue – Sagelie R 1983

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Rate of bone loss

Loe et.al 1986 – study in Sri lankan tea labors

Bone loss 0.2mm on facial and 0.3mm for proximal surface per

year

8% rapid bone loss – 0.1-1.0mm

81% moderate bone loss – 0.05-0.5

11% minimal bone loss – 0.05-0.09

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Lipopolysaccahrides mediated bone destruction

LPS – initiation of host response

Recruitment of immuno-inflammatory cells and activation of

Osteoclasts – Genco CA 2004

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Effect of Prostaglandins

PG bone loss associated with periodontitis – Zubery et al 1998

NSAID’s less bone loss – Willams RL 1985

NSAID’s reduces development of gingivitis and alveolar bone

loss – Howell 1993

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Trauma from occlusion

Trauma in absence of inflammation

Trauma combined with inflammation

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Glickman’s concept(1965)

The pathway of the spread of a plaque-associated gingival lesion can be changed if forces of an abnormal magnitude are acting on teeth harboring subgingival plaque

Waerhaug’s concept(1979)

Angular bony defects & infrabony pockets occur equally at periodontal sites of teeth which are not affected by TFO

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Bone loss in periodontitis

Chronic periodontitis

Aggressive periodontitis

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Bone in Diabetes

Diabetes decreases gene expression of osteoblasts – Bouillon

1991

AGE’s inhibits osteoblast differentiation – Mc Carthy et al 2001

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Bone destruction patterns

Horizontal bone loss

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Vertical or angular bone defects

Lindhe 1982 – vertical defects increases with age

Glickman 1961- 3 wall defect, mesial lower molars

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Goldman and Cohen 1958

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Osseous craters

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Bulbous bone contour

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Reverse bone architecture and ledges

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Exostoses

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Trench

Loss of alveolar bone and a portion of supporting alveolar bone

in two or three surface of tooth

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Moat

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Ramp

Loss of alveolar bone and supporting bone, but margins being at different levels

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Furcation involvement

Larato 1970 – mandibular 1st molar most common maxillary pre

molars least common

No. furcation involvement increases with age

Tal H 1984 – high prevalence in upper molars

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Classification

Irving Glickman 1953

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 Hamp, Nyman & Lindhe`s Classification (1975)

Horizontal destruction of supporting bone

Class I, II, III

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Tarnow and Fletcher(1984)

Grade A – Vertical loss of 1 – 3mmGrade B – Vertical loss of 4 – 6 mmGrade C – Vertical Loss of 7 + mm

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Bone loss after flap surgery

2mm of flap reflection – 0.5mm bone loss

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Bone around implant

•Osseointegration•Osseoperception from bone

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Therapeutic approaches to treat pathological bone loss

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NSAID’s

Bisphosphonates

TNF α antagonists

Interleukin antagonists

RANK / RANKL interaction inhibitors (DENOSUMAB –

monoclonal antibody)

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Bone grafts

Auto grafts

Allografts

Xenografts

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Guided bone regeneration

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Conclusion

In healthy bone processes are coupled by complex interplay of

osteoblasts and osteoclasts along with local and systemic

biochemical, as well as biomechanical factors. Knowledge of

bone loss and its causes associated with periodontal disease gives

us insight for successful treatment

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References

Carranza 10th edition Orbans – Text book of oral histology 12th edition Lindhe 5th edition Connective tissue of periodontium – Mark Bartold, Sampath narayanaMolecular and cellular biology of alveolar bone. Jaro and McKee.

Perio2000; 24; 2000; 99-126.The extracellular matrix of periodontium. Angelo Mariotti, Perio

2000:3,1993;39-63Mechanism and control of pathologic bone loss in periodontitis, Mark

Bartold Perio 2000: 53, 2010, 55-69Mechanism of alveolar bone destruction in periodontitis. Schwartz,

perio 2000:14,1997, 158-172