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1. ALVEOLAR BONE IN HEALTH AND DISEASE
1. INTRODUCTION
2. OBJECTIVE
3. BONE IN GENERAL
CLASSIFICATION OF BONES
STRUCTURE OF BONE
OSSIFICATION METHODS
GROWTH OF BONE
4. ALVEOLAR BONE
5. ANATOMY OF ALVEOLAR BONE
6. FUNCTIONS
7. EMBRYOGENESIS
8. STRUCTURAL HEIRARCHY
9. REMODELLING AND REPAIR
10. MECHANISM OF BONE RESORPTION
11. ALVEOLAR BONE IN DISEASE
12. CONCLUSION

2. INTRODUCTION:
Alveolar bone is a specialized part of the mandibular and maxillary bones that
forms the primary support structure for teeth. Although fundamentally comparable to
other bone tissues in the body, alveolar bone is subjected to continual and rapid
remodeling associated with tooth eruption and subsequently the functional demands
of mastication. The ability of alveolar bone to undergo rapid remodeling is also
important for positional adaptation of the teeth but may be detrimental to the
progression of periodontal disease. Much of the current information on alveolar bone
must be extrapolated from studies of other bone tissues.
BONE IN GENERAL:
There are two types of bone tissue: compact and spongy. The names imply
that the two types of differ in density, or how tightly the tissue is packed together.
Compact Bone
Compact bone consists of closely packed osteons or haversian systems. The
osteon consists of a central canal called the osteonic (haversian) canal, which is
surrounded by concentric rings (lamellae) of matrix. Between the rings of matrix, the
bone cells (osteocytes) are located in spaces called lacunae. Small channels
(canaliculi) radiate from the lacunae to the osteonic (haversian) canal to provide
passageways through the hard matrix. In compact bone, the haversian systems are
packed tightly together to form what appears to be a solid mass. The osteonic canals
contain blood vessels that are parallel to the long axis of the bone. These blood
vessels interconnect, by way of perforating canals, with vessels on the surface of the
bone.

3. ALVEOLAR PROCESS
The alveolar process is the part of maxilla or mandible that forms and supports
the teeth. As a result of functional adaptation, two parts of alveolar process may be
distinguished.
1. The alveolar bone proper (socket wall)
The alveolar bone proper consists of thin lamella of bone (cortical bone)
surrounding the root and bundle bone. Sharpey’s fibers of periodontal ligament are
embedded in bundle bone. Some sharpey’s fibers are calcified completely, but most of
them contain a central uncalcified core.
2. The supporting bone.
The supporting bone surrounds the alveolar bone proper and provides
additional functional support. Supporting bone consists of (1) the compact cortical
plates of vestibular and oral surfaces of alveolar processes (outer cortical plates) and
(2) the cancellous, trabecular, or spongy bone sandwiched between these cortical
plates and the alveolar bone proper (inner cortical plate).
In roentgenograms the alveolar bone proper appears as an opaque line called the
lamina dura. The alveolar bone proper is perforated by many openings through which
the blood vessels, lymphatics and nerves of periodontal ligament pass. It is also called
the cribriform plate because of perforations. The inner cortical plate contains the
sharpey’s fibers of periodontal ligament fibers.
The inner and outer cortical plates meet at alveolar crest where they may fuse.
The inner cortical plates of adjacent alveoli are also fused interdentally. The alveolar
crest more or less parallels the outline of the cervical margin of the enamel 1-3mm
apical to it, with a greater distance seen in older individuals.
The interdental septa are the bony partitions that separate adjacent alveoli.
Coronally, at the cervical region, the septa are thinner and here the inner cortical
palates are fused and cancellous bone is frequently missing. Apically the septa are
thicker and generally contain intervening cancellous bone and some times haversian
bone.
The shape of the alveolar crest, under normal conditions, depends on the
contour of enamel of adjacent teeth, the relative position of the adjacent CEJ, the
degree of eruption of teeth, the vertical positioning of the teeth, and the oro-vestibular
depth of the teeth. In general, the bone about each tooth follows the contour of the
cervical line.

4. FUNCTION:
The alveolar bone proper adapts itself to the functional demands of the teeth in
a dynamic manner. It is formed for the express purpose of supporting and attaching
the teeth. The alveolar process depends on the presence of teeth for its existence. If
teeth fail to develop, it will not form. If teeth are lost or extracted, it will tend to
involute.
ANATOMY:
Roentgenograms
Roentgenograms of cross-sections of the alveolar process show its cortical and
cancellous portions. The cortical plates are generally thicker in the mandible. The
cortical plates and the cancellous bone are also generally thicker on the oral aspects of
the mandible and the maxilla, but there is individual variation.
Anteriorly, along the vestibular aspect of the alveolar arch, is the depression of
the incisive fossa, bordered distally by the cuspid eminences. Here the bone is thin,
and there may be little or no cancellous bone. Posteriorly, in the premolar and molar
regions, the bone is thicker, and generally, cancellous bone separates the cortical plate
from the alveolar bone proper.
Thickness of alveolar process
Since the teeth are responsible for the alveolar process, it general form and
shape follow the arrangement of the dentition. In addition the thickness of alveolar
bone has a direct bearing with external contour. When the process is thin interdental
depressions can be seen between roots and there are prominences over roots.
Malposition of teeth also affects the thickness of alveolar process.
Alveolar crest:
The margin of alveolar process is normally rounded or beaded. Occasionally
the margin ends in fine sharp edge. This occurs when the bone is extremely thin for
example on the vestibular surface of incisors and canines.
The contour of crestal bone margin is generally scalloped. If root surface is
flat then crest is also flat. If root surface has convex surface then crestal bone margin
follows convexity giving scalloping appearance.
Form of interdental septum
The form of interdental septum follows the alignment of adjacent CEJs. The
septa in anterior region form peaks. In posterior region they are wide and flat. When
the teeth are in close approximation the interdental septa is absent. This is seen mostly
between the distobuccal root of maxillary 1st
molar and mesiobuccal root of adjacent
second molar. The distance between crest of alveolar bone to CEJ in young adults
varies between 0.75 – 1.49. This distance increases with age to an average 2.81.

5. Relationship with maxillary sinus:
The maxillary sinus is separated from the root apices of molars in maxilla by
thin osseous partition. With the age sinus grows towards roots decreasing the
thickness of this partition. After extraction of molar the sinus grows more rapidly. The
cortical plate between teeth next to extraction socket and the sinus may become paper
thin. This may lead to oroantral fistulas during surgical procedures involving such
regions.
Dehiscence & Fenestrations
Dehiscence is dipping of crestal bone exposing the root surface. Fenestration
is circumscribed hole in the cortical plate over the root and does not communicate
with crestal margin. It varies in size and can be located any where along the root
surface.
EMBRYOGENESIS OF ALVEOLAR BONE:
The alveolar bone of maxilla is formed by mesenchyme. The mandibular
alveolar bone develops from the mesenchyme of first branchial arch initially adjacent
to Meckel’s cartilage. The genesis of alveolar bone is similar to intramembranous
ossification else where in the body.

6. Mesenchymal cells form aggregations that differentiate into osteoblasts.
According to Newman this is in response to adhesion molecules (eg, fibronectin) and
soluble signals. These two are members of transforming growth factor –beta (TGF-β)
family. The regional proclivity for direct, intramembranous bone formation in
mandibulocranial complex has not yet been explained satisfactorily. It is accepted that
bone morphogenic proteins (BMPs), a subgroup within TGF-β family promote
osteoblastic differentiation from mesenchymal cells. Perhaps there is a concentration
gradient of BMPs that favors intra membranous bone formation in this area during 5th
and 6th
week of gestation. Ripamonti described that basic FGF on the surface of
vascular endothelium, type IV collagen and matrix components of blood vessels bind
to BMP-3, BMP-4 and BMP-7. Thus the BMPs concentration gradient is greater in
the mandibulocranial complex. Where as in endochondral bone sites angiogenesis
inhibitors (protamine) down regulates the bFGF synthesis. This diminishes vasularity
in endochondral bone forming sites and cartilage is formed as described by Taylor
and Folkman. Other factors that may inhibit vascularisation here are interferon-β, IL-
12, angiostatin.
Osteoblasts secrete matrix vesicles. The process of calcifying extracellular
matrix begins in the centre of spherule of aggregated osteoblasts, collagen,
proteoglycans, and matrix vesicles. The first sign of hydroxyapatite calcification is
seen within matrix vesicle. Later hydroxyapatite crystals growing by epitaxy form
spheroids. These are bone nodules that coalesce into seams of woven bone and extend
in, on and between collagen fibrils. As the first deciduous tooth buds appear in
maxilla and mandible, Woven bone spicules loosely surround each developing tooth.
Trabeculae of woven bone grow and anastomose. The osteoblasts are trapped in
growing calcified matrix and are now termed osteocytes.

7. On the trabecular surfaces of woven bone, collagen is secreted in oriented
sheets that calcify by epitaxy from the hydroxyapatite crystals in the woven bone. The
successive layers of collagen, each sheet oriented in different plane, give the bone
leaflet-on-leaflet appearance called lamellar bone. Shortly after the first woven bone
has formed, osteoclasts are found on the surfaces of both the woven and lamellar bone
of trabeculae. They begin the process of resorption and with osteoblasts, remodeling
the bone into its proper shape at each stage of development.
STRUCTURAL HIERARCHY OF ALVEOLAR BONE:
Microstructure: alveolar bone may be categorized into four microstructural
components: cells, inorganic matrix, organic matrix and soluble signaling factors.
Bone cells: bone cells include Osteoblasts, Osteocytes, and Osteoclasts.
1. OSTEOBLASTS:
Osteoblasts are derived from mesenchymal lineage. Actively secreting
osteoblasts are lined up along the osseous surface as sheet of plump,
basophilic cells with large nuclei. They have well developed Golgi regions
with a dense network of rough –surfaced endoplasmic reticulum. Ctyoplasmic
extensions may traverse the osteoid layer to make contact with those of
adjacent osteocytes. Where active osteogenesis is absent, the bone surface may
be lined with flattened cells lacking a rough endoplasmic reticulum. They are
considered to be osteoprogenitor cells. They are capable of dividing into
preosteoblasts, which no longer able to divide and may evolve further into
osteoblasts.
The progression of stem cells to end stage osteoblasts may take two
roots one leading to determined osteoprogenitor cells. The determined lineage
is associated with cell condensation and may be responsible for bone
formation during embryogenesis, whereas during fracture repair an inducible
population may be susceptible to soluble inductive morphogens- polypeptides
that promote expression of distinctive cell phenotypes. The effect being dose
related.
When bone is injured as a consequence of surgical intervention and
trauma, a population of local cells restores osseous form and function through
recapitulation of embryonic events the local cells are determined
osteoprogenitor, resident in the cambial layers of the periosteum, endosteum
and dura, and inducible osteoprogenitor cells, such as pericytes that arrive at
injury locus about 3-5 days after injury via transit in developing capillary
sprouts. Pericytes also may convert to osteoblasts following interactions with
endogenous BMPs.
Further more, according to Brighton and colleagues, a population of
polymorphic mesenchymal cells may appear as early as 12 hours following

8. fracture, providing a preosteoblastic cell resource. Moreover mesenchymal
stem cells within the bone marrow contribute to the complement of cells
present within the repair blastema. These cells, which possess multilineage
potential, can convert either to cartilage – forming chondrocytes or bone
-forming osteoblasts depending on the presence of environmental cues such as
nutrients supply, specific growth factors, blood vessels and mechanical
stability. It already has been established that marrow-- derived inducible
osteoprogenitor cells undergo osteoblastic differentiation in response to BMPs
and other naturally occurring growth factors.
The osteoblasts secrete soluble signaling factors eg, BMPs, TGF-β,
insulin like growth factor I and II, interleukin-1 and platelet derived growth
factors and osteoid. For remodeling the osteoid produced is produced at the
rate of 2-3µm/ day at a thickness of 20 µm. the osteiod mineralizes at the rate
of 1-2µm/day.
2. OSTEOCYTES:
Osteocytes are derived from osteoblasts and are capable of resorbing
and forming bone. Osteocytes have reduced cytoplasm and cellular organelles
when compared to osteoblasts. Their Ctyoplasmic processes radiate from the
cell body though numerous canaliculi to connect with cells in adjacent
lacunae. Osteocytes respond to changing hormonal levels. They are able to
resorb bone lacunar walls (osteocytic osteolysis) and to deposit new bone.
Osteocytes are relatively inactive cells, yet their subdued metabolic
activity is crucial to bone viability and sustain homeostasis (maintenance of
constant internal conditions within the body). All the three cells of bone play
important role in calcium regulation, homeostasis, remodeling and repair.
Their life span is for many years, perhaps even decades.
3. OSTEOCLASTS:
Osteoblasts are multinucleated cells in depressions of bone surface.
They are the main cells capable of bone resorption. The surface facing bone is
highly convoluted forming a “ruffled border.” The cytoplasm of osteoclasts
contains numerous vesicles, lysosomes, and mitochondria, but little
endoplasmic reticulum. The size and concentration of vesicles increase in
proximity to the ruffled border, which is the zone where active bone resorption
takes place. Free apatite crystallites and frayed collagen fibrils are found
between the Ctyoplasmic extensions of these cells. The periphery of the
ruffled border, by contrast, closely contacts the bone surface and seals the
resorptive, ruffled border zone. This region is referred to as the clear zone
because the adjacent cytoplasm lacks organelles and particulate elements. The
cavities formed after resorptions are called Howship lacunae.
They originate from macrophages of hemopoietic origin. These cells
fuse to form typical multinucleated cells or they may participate in bone
resorption as single nuclear cells. Fibroblast derived collagenase also
contribute to bone resorption.

9. The number of osteoblasts may be increased by parathyroid hormone
and is decreased by calcitonin. 1, 25-Dihydroxycalciferol increases the
resorptive activity without increasing cell number. In addition to these local
factors such as osteoclasts- activating factor (OAF), lymphokines (IL-1, -3,-6,
and -11) and prostaglandins also influence bone resorption
BONE MATRIX:
The matrix of bone is of two types i.e. organic and inorganic matrix.
Organic matrix:
The organic matrix constitutes 35% of dry weight of bone. It can be
divided into collagenous and noncollagenous components. Collagenous part
contains type I collagen (about 90%). They form fibrous backbone of extra
cellular matrix (ECM). The rest 10% are noncollagenous proteins. They
include proteoglycans, glycoproteins and BMPs.
The proteoglycans are composed of glycosaminoglycans (GAGs)
covalently linked to core proteins. The GAGs contain repeating carbohydrate
units that are sulfated; eg, chondroitin sulfate, dermatan sulfate, keratin
sulfate, hyluronic acid and heparin sulfate. The examples of proteoglycans are
fibromodulin, osteoadherin, osteoglycin. Examples of glycoproteins are
fibronectin, osteonectin, osteopontin, fibrilin. These noncollagenous proteins
may modulate cellular attachment.

10. The ability of bone to induce new cartilage and bone formation is from
the action of the BMPs.
Inorganic matrix:
It constitutes for 60-70% of dry weight of bone i.e. 2/3 of matrix. The
inorganic matter is composed principally of minerals calcium, phosphate along
with hydroxyl, carbonates, citrate and trace amount of other ions, such as
sodium, magnesium, and fluorine. They form hydroxyl apatite crystals
Ca10 (PO4)6(OH) 2. These apatite crystals are arranged parallel to the long axes
of collagen fibers and appear to be deposited on and within these fibers. In this
fashion the bone can withstand the heavy mechanical stresses applied to it
during function.
REMODELING AND REPAIR OF BONE:
In normal physiology, there is a coupling of resorption and formation
in the bone remodeling sequence. In the various metabolic bone diseases, there
are abnormalities in the coordinated activity of the osteoclastic and
osteoblastic cells. Likewise, in a pathological state such as inflammation, there
is an uncoupling of these activities resulting in a net loss of bone. A complex
cascade of events involving a host of autocrine and paracrine factors is
involved in the regulation of bone metabolism.
The structure of alveolar bone proper varies on different sides of tooth,
with different functional demands. Under physiologic conditions teeth migrate
continuously in mesial direction toward the midline. This is called physiologic
mesial drift. The migration leads to resorption on mesial side and new bone
formation on tension side i.e., distal side.
Some portions of bone surface may be covered by a thin layer old new
bone that anchors short sharpey’s fibers. This new bone is formed during
relatively brief periods of bone deposition, which allows the root to remain

11. anchored to bone despite a predominance of bone resorption over deposition.
This new bone is separated from old bone by reversal line. Reversal lines tend
to have scalloped outline that separates them last resorptive activity area. This
outline is result of resorptive bays created by osteoclasts.
MECHANISM OF BONE RESORPTION
1. Hydrolytic enzyme mechanism
2. Acidic environment mechanism or proton pump mechanism
Ultrastructural evidence suggests that osteoclasts first solubilize the
mineral phase and next cause dissolution of the organic phase of the matrix.
The resorption area is defined beneath the ruffled border as a highly
specialized region of cytoplasmic infolding on the plasma membrane, outlined
by a sealing zone or clear zone. The clear zone has been shown to contain
podosomes, specialized protrusions of the ventral membrane of osteoclasts,
which adhere to the calcified substrate to be broken down. It has been
demonstrated that the clear zone contains a network of actin-containing
microfilaments. It has been demonstrated that lowering of extracellular
calcium promotes podosome formation, but raising intracellular calcium by
blocking the calcium pumps induces podosome disappearance and formation
of membrane ruffles. An electrogenic H + -transporting, ATPase-driven
proton pump similar to renal tubular epithelial transport systems establishes a
pH gradient. Intracellular pH regulation is most likely achieved by carbonic
anhydrase which has been shown to be abundant in osteoclast cytoplasm.
Bicarbonate, generated by this carbonic anhydrase, appears to be secreted
from the basolateral membrane via HCO3/CL- exchange. The protons released
into the functionally extracellular lysomal compartment may solubilize bone
mineral and create a suitable pH for lysosomal enzyme activity on the
demineralized organic bone matrix.
ALVEOLAR BONE IN DISEASE:
The alveolar bone destruction can be divided into following types:
1. Bone destruction caused by extension of gingival inflammation.
2. bone destruction caused by trauma from occlusion
3. bone destruction caused by systemic disorders
Bone destruction caused by systemic disorders:
Osteopenia / osteoporosis:
Osteopenia is characterized by a reduction in bone mass, whereas osteoporosis
is the most severe degree of osteopenia which leads to pain, deformity, or fracture.
Osteoporosis is a physiological, gender, and age-related condition resulting from bone
mineral content loss and structural change in bones. The rate of bone mineral loss is
approximately two times greater in women than men. In women, post-menopausal
osteoporosis is a heterogeneous disorder which begins after natural or surgical
menopause

12. Alveolar Bone Loss Progression in Diabetes:
It suggested that poorer glycemic control leads to both an increased risk for
alveolar bone loss and more severe progression over those without type 2 DM.
1. Polymorphonuclear Leukocyte Function.
2. Collagen Metabolism and Advanced Glycation End products.
Vitamin D deficiency:
Vitamin D or calciferol is essential for the 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.
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.
Sex hormones:
Ovirectomy results in osteoporosis of alveolar bone, reduced cementum
formation, and reduced fiber density and cellularity of periodontal ligament in young
adult mice, but not in older animals. The gingival epithelium is atrophic in estrogen-
deficient animals.
Systemic administration of testesterone retards the down growth of sulcular
epithelium over cementum, stimulates osteoblastic activity in alveolar bone; increases
the cellularity of periodontal ligament; and restores osteoblastic activity, which is
depressed by hypophysectomy
Hematological disorders:
In leukemic mice , 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.
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. On the other way periodontal infections may precipitate
sickle cell crisis.

13. Conclusion:
Bone mass represents the balance of bone formation and bone resorption. In
health, these processes are coupled by complex interplay of local and systemic
biochemical, as well as biomechanical control of osteoblasts and osteoclast activity.
Various diseases alter this balance. In osteoporosis, for example, bone resorption
outweighs bone formation, and a net loss of bone is revealed by the reduction of bone
mass and susceptibility to fracture. In states where there is high bone turnover
(increased osteoclast activity), treatment by hormone replacement therapy (estrogens),
bisphosphonates and more infrequently calcitonin aims to reduce the number of
resorptive osteoclasts. In states where there is low turnover (deficient osteoblasts
activity), a number of experimental protocols, including fluoride and intermittent
parathyroid hormone treatment, suggest that osteoblast activity can be enhanced to
improve bone mass. General approaches to maintaining bone mass focus on proper
nutrition and intake of calcium and vitamin D, maintenance of menses and weight-
bearing exercise. Does pathologically reduced osteoblast activity or elevated
osteoclast activity impact bone formation and maintenance in dental alveolar bone
regeneration
References:
1. Clinical Periodontology by Carranza, Newman and Takei.
2. Periodontics by Grant, Stern and Listgarten.

14. Alveolar Bone
Seminar by
Dr. N.Upendra Natha Reddy
Postgraduate Student
2004-2007