This document discusses the cells and components that make up healthy alveolar bone. It describes the main cell types, including osteoprogenitor cells that develop into osteoblasts or osteoclasts. Osteoblasts secrete osteoid and regulate mineralization, while osteoclasts are responsible for bone resorption. The bone matrix contains collagen fibers and hydroxyapatite crystals, along with noncollagenous proteins. Alveolar bone undergoes physiological remodeling through the coordinated actions of osteoblasts and osteoclasts, allowing adaptation to tooth movement and replacement over time.

1. Alveolar Bone in Health
Part - B
Dr. Ibrahim Shaikh
Dept. of Periodontology & Implantology
Seminar No. 6
10/08/2015
Guide : Dr.Varsha Rathod

2. 1. Cell types in bone
2. Matrix components
3. Ultrastructural organization
4. Physiologic remodelling of alveolar bone
5. The implant - bone interface
6. Conclusion
7. References
2
CONTENTS

3. 3
CELLTYPES

4. ▪ The cells that eventually give rise to osteoblasts are termed
osteoprogenitor cells.
▪ Reside in the layer of cells beneath the osteoblast layer in the
periosteal region, in the periodontal ligament, or in the marrow
spaces.
▪ Fibroblast-like cells, with an elongated nucleus and few
organelles.
▪ Life cycle-up to about eight cell divisions.
OSTEOPROGENITOR CELLS

5. Friedenstein (1973) divided osteoprogenitor cells into;
 Determined osteogenic precursor cells are present in bone
marrow, in the endosteum and in the periosteum that cover
the surfaces of the bone. These cells possess an intrinsic
capacity to proliferate and differentiate into osteoblasts.
 Inducible osteogenic precursor cells represent mesenchymal
cells present in the other organs and tissues (e.g. muscles)
that may become bone forming cells when exposed to
specific stimuli.
OSTEOPROGENITOR CELLS

6. OSTEOBLASTS
▪ These are specialized fibroblast-like cells of mesenchymal
origin.
▪ Basophilic, plump cuboidal or slightly flattened,
mononucleated cells.
▪ Contain a cytoplasm rich in synthetic and secretory organelles
as rough ER, Golgi apparatus, secretory granules and
microtubules
6

7. ▪ Secretes- Osteoid
▪ unmineralised bone matrix
▪ thickness –5-10  before reaching a level of maturity
conducive to mineralisation.
▪ consists of type 1 collagen fibres, more or less parallel to
bone.
▪ There is a lag phase of about 10 days before the deeper
layer of osteoid has matured sufficiently to undergo
mineralisation
7
OSTEOBLASTS

8. Functions of osteoblasts
 Secretion of osteoid and control of mineralization of bone.
 Production of paracrine and autocrine factors.
 Production of proteases, which are involved in matrix
degradation.
 Expression of RANKL, whose presence is vital in osteoclast
differentiation.
OSTEOBLASTS

9. Osteoblasts control the process of mineralization at three
levels:
1. Primary calcification, by production of an extracellular
organelle called the matrix vesicle
2. Secondary calcification, by modifying the matrix
through the release of different enzymes
3. By regulating the amount of ions available for mineral
deposition in the matrix
OSTEOBLASTS

10.  Cover most but not all inactive bone surfaces
 Decreased protein secretion
 Relative paucity of organelles
By covering the surface of bone, they protect it from any
resorptive activity from osteoclasts.
They may also be reactivated to form osteoblasts.
Inactive surfaces are known to be a primary site of mineral ion
exchange between blood and adult bone.
BONE LINING CELLS

11.  ‘Entrapped osteoblasts’
 About 25000 osteocytes per cubic millimeter of bone
 Decreased quantity of secretory organelles
 Smaller size with large nucleus
 Formative and resorptive activity of these cells may vary under
certain metabolic requirements-”OSTEOCYTIC OSTEOLYSIS”
 Numerous cell processes from the osteocytes run in the
canaliculi in all directions.
 Detect stresses induced in bone and are regarded as the main
mechanoreceptors of bone.
OSTEOCYTES

12. Horizontal section of bone demonstrating a layer of osteoblasts (A) lining a surface where
active bone formation is occurring (as indicated by the presence of a pale staining layer of
osteoid), some large multinucleated osteoclasts (B) lying against Howship's lacunae in a
region of bone undergoing resorption, and large numbers of osteocytes (C) lying
embedded within the bone matrix itself. D - Bone-lining cells; E - pale-staining osteoid layer

13.  They are derived from haemopoietic cells of the monocyte/
macrophage lineage by fusion of mononuclear precursors,
giving rise to multinucleated cells.
 Osteoclasts are the cells responsible for bone resorption
 Howship’s lacunae : bony concavities
 Osteoclasts may be up to 100 um in diameter and have on
average 10-20 nuclei.
 The lifespan of osteoclasts is thought to be about 10-14
days.
OSTEOCLASTS

14.  Part that lies adjacent to bone – foamy striated appearance
(the so called ruffled –border).
 Marker for osteoclasts – Tartrate resistant acid phosphatase
(TRAP)
 Osteoclasts are recruited only when required.
OSTEOCLASTS

15. 15
OSTEOBLASTS & OSTEOCLASTS

16.  The bone matrix is formed from a scaffold of interwoven
collagen fibers within and between which small, uniform,
plate-like crystals of carbonated hydroxyapatite
(Ca10[PO4]6[OH]2) are deposited.
 Other proteins, including proteoglycans, acidic glycosylated
and non-glycosylated proteins associate with and regulate
the formation of collagen fibrils and mineral crystals, or
provide continuity between matrix components and between
the matrix and cellular components.
MATRIX COMPONENTS

17.  Small amounts of carbohydrate and lipid contribute to the
organic matrix - comprises 1/3rd of matrix.
 Calcium and phosphate in the form of poorly crystalline,
carbonated apatite, also described as dahllite, predominates
the inorganic phase.
MATRIX COMPONENTS

18.  Collagen comprises the major ~80–90% organic component.
 The collagen fibrils in bone are stabilized by intermolecular
cross-linking involving lysines and modified lysines that form
pyridinium ring structures (pyridinolines) - high tensile strength
 In rapidly forming (woven) bone that is produced during early
development and in repair sites, the fibers are extensively
interwoven, leaving a substantial volume of inter-fibrillar space
that is largely occupied by mineral crystals and associated acidic
proteins.
COLLAGEN

19.  Osteocalcin and bone sialoprotein, are essentially unique to
mineralized tissues, whereas others, such as osteonectin/ SPARC
and osteopontin have a more general distribution.
 These proteins are released from bone by demineralization,
reflecting the predominant association with the mineral phase..
 Certain proteins derived from blood and tissue fluids are
concentrated in bone include albumin, α2HS-glycoprotein,
immunoglobulins and matrix gla protein.
NONCOLLAGENOUS PROTEINS

20. PROTEIN KNOWN FUNCTION
REGULATIONOF
PRODUCTION
Osteocalcin
Inhibits mineralization, recruit bone cell
precursors.
1,25-(OH)2 D3, PTH,
Glucocorticoids
Osteonectin
Facilitate type 1 collagen mineralization,
suppress rate of hydroxyapatite crystal
growth, modulate cell attachment and
detachment
Glucocorticoids,
TGF-β, IGF-1
Osteopontin
Cell binding activity, osteoclast anchoring
& mineral binding activity.
1,25-(OH)2 D3, PTH,
Glucocorticoids, TGF-β,
retinoic acid
Bone sialoprotein Cell binding activity
1,25-(OH)2 D3,
Glucocorticoids
NONCOLLAGENOUS PROTEINS

21. PROTEIN KNOWN FUNCTION
REGULATIONOF
PRODUCTION
Bone proteoglycan
(biglycan)
Function unclear Not well characterized
Bone proteoglycan-2
(decorin)
Bind to collagen fibers, regulate fiber
growth, bind/present growth factors in
matrix.
Not well characterized
Thrombospondin Bind and organize matrix, cell attachment TGF-β
Matrix gla - protein Prevent growth plate mineralization
1,25-(OH)2 D3, retinoic
acid
NONCOLLAGENOUS PROTEINS

22.  Complete remodeling of the alveolar bone occurs when the
primary dentition is replaced by succedaneous teeth.
 The ability of the alveolar bone to remodel rapidly also
facilitates positional adaptation of teeth in response to
functional forces and in the physiological drift of teeth that
occurs with the development of jaw bones.
 Formation of alveolar bone is a prerequisite for the
regeneration of tissues lost through periodontal disease and
for osseointegration of implants used in restorative dentistry.
REMODELLING OF ALVEOLAR BONE

23. 23
REMODELLING OF ALVEOLAR BONE

25.  Formation of bone, which appears to be linked with bone
resorption to maintain bone mass, involves the proliferation
and differentiation of stromal stem cells along an
osteogenic pathway that leads to the formation of
osteoblasts.
 The formation of a collagen substratum appears to trigger
the differentiation of pre-osteoblastic cells into osteoblasts
through interactions with the α2β1 receptor.
BONE FORMATION

26.  Tencate, described the sequence of events in the resorptive
process as follows:
1. Attachment of osteoclast to the mineralized surface of
bone.
2. Creation of a sealed acidic environment through the action
of the proton pump, which demineralizes bone and exposes
the organic matrix.
3. Degradation of exposed organic matrix to its constituent
amino acids by the action of released enzymes, such
as acid phosphatase and cathepsin B.
4. Sequestering of mineral ions and amino acids within the
osteoclast.
BONE RESORPTION

27. REGULATION OF OSTEOCLAST ACTIVITY

28.  During the growth of maxilla and the mandible, bone is
deposited on the outer surfaces of the cortical plates.
 In the mandible, with its thick, compact cortical plates, bone
is deposited in the shape of basic or circumferential
lamellae. When the lamellae reach certain thickness, they
are replaced from inside by haversian bone. This
reconstruction is correlated to the functional and nutritional
demands of the bone.
INTERNAL RECONSTRUCTION OF BONE

29.  In the haversian canals, closest to the surface; osteoclasts
differentiate and resorb the haversian lamellae and part of
circumferential lamellae.
 The resorbed bone is replaced by proliferating loose connective
tissue. This area of resorption is sometimes called the cutting cone
or the resorption tunnel
 After a time the resorption ceases and the new bone is opposed
onto the old. The scalloped outline of howship's lacunae that turn
their convexity toward the old bone remains visible as a darkly
stained cementing line, a reversal line.
 This is in contrast to those cementing lines that correspond to a rest
period in an otherwise continuous process of bone apposition. They
are called resting lines.
INTERNAL RECONSTRUCTION OF BONE

31.  The relationship between endosseous implants and bone
consist as of one of the two mechanism:
1. Osseointegration: when the bone is in intimate but not
ultrastructural contact with implant or,
2. Fibrosseous integration, in which soft tissues such as
fibers and/or cells, are interposed between the two
surfaces.
 Osseointegration concept proposed by Branemark et al
 Called functional ankylosis by Schroeder; he states that
there is an absence of connective tissue or any non-bony
tissue in the interface between the implant and the bone.
THE IMPLANT-BONE INTERFACE

33.  After implant insertion; First, woven bone is quickly
formed in the gap between the implant and bone.
 Second, after several months, this is progressively replaced
by lamellar bone under the load stimulation.
 Third, a steady state is reached after about 1 ½ years.
Often for oral implants, occlusal load is allowed as soon as 2-
3 months, while mostly woven bone is present.
THE IMPLANT-BONE INTERFACE

34. THE IMPLANT-BONE INTERFACE

35.  Alveolar bone, which has interdependence with the
dentition, has a specialized function in the support of the
teeth. While there are architectural specifications for
alveolar bone that relate to its functional role, the basic
cellular and matrix components are consistent with other
bone tissues. Similarly the cellular activities involved in the
formation and remodelling of the alveolar bone and the
factors that influence these cellular processes are common
to bone tissues generally. However, specific features, such
as the rate of remodelling, may be unique to alveolar bone
and may be important for its adaptability.
CONCLUSION

36. 1. Clinical periodontology; Newman, Takei, Klokkevold, Carranza; 10th edn
2. Oral anatomy, histology and embryology; Berkovitz, Holland, Moxham;
3rd edn
3. Tencate’s Oral histology- development, structure and function; Antonio
Nanci; 6th edn
4. Orban’s Oral histology and embryology; S.N.Bhaskar; 10th edn
5. Clinical periodontology and implant dentistry; Jan Lindhe; 4th edn
6. Jaro sodek&marc D.mckee; Molecular and cellular biology of alveolar
bone; Periodontology 2000, Vol. 24, 2000, 99–126
7. Moon-il cho & Philias r. garant; Development and general structure of the
periodontium; Periodontology 2000, Vol. 24, 2000, 9–27.
REFERENCES

37. THANK YOU