Introduction

Terminologies
Classification Composition

Development
Structure of alveolar bone Cell types

Bone Remodeling

 PERIODONTIUM:

The term perodontium is derived from the terms perio and odont .
Perio means Around and Odont means Tooth.

 The tissues that invest and support the teeth including

the gingiva, alveolar mucosa, cementum, periodontal ligament and the supporting alveolar bone. (GPT 2001)
The periodontium is defined simply as the tissues

investing and supporting the teeth

(Dorlands illustrated medical dictionary. 24th edition. Philadelphia: Saunders, 1965: 1129.)

 The Gingiva The periodontal ligament

Alveolar bone
The cementum

 There are in all 206 bones in the adult human skeleton.

Definition: The hard form of connective tissue that constitutes the majority of the skeleton of most vertebrates. It consists of an organic component and an inorganic, or mineral, component. The organic matrix contains a framework of collagenous fibers and is impregnated with the mineral component, chiefly calcium phosphate and hydroxyapatite, that imparts rigidity to bone. The alveolar process supports to alveoli, and consists of cortical bone, cancellous trabeculae, and the alvolar bone proper. (Glossary of Periodontal Terms 2001)

The alveolar process is the portion of the maxilla and mandible that forms and supports the tooth socket (alveoli).

Alveolar bone proper is the inner socket wall of thin, compact bone. Cribriform plate series of perforations/openings in the alveolar bone proper

Lamina dura radiological term used to describe the cribriform plate Bundle bone bone adjacent to the periodontal ligament that contain a greater number of Sharpeys fibres (Schroeder 1992) Interdental septum is that part which separates the individual alveoli. It consists of cancellous bone enclosed within the compact border.

 Compact bone is dense and forms the surface of

bones, is extremely hard, formed of multiple stacked layers with few gaps
Cancellous bone (also known as trabecular, or

spongy) is a type of osseous tissue with a low density and strength but very high surface area, that fills the inner cavity

According to position Axial Appendicular According to shape Long bones Short bones Flat bones Irregular bones Pneumatic bone Sesamoid bone

According to development Endochondral ossification Intramembranous ossification Sutural According to magnifications As seen with naked eye: - compact bone spongy bone

High powered lens :- coarse fibered woven bone fine fibered lamellar bone

BONE

Inorganic (65%)

Organic (35%)

Hydroxyappatite Collagen (88-89%) Noncollagenous (11-12%)

Glycoproteins (6.5-10%) Proteoglycans (0.8%) Sialoproteins (0.35%) Lipids (0.4%)

 Intramembranous

Endochondral
Sutural

 Here bone develops directly with the soft tissue

membrane rather that on a cartilaginous model.

Embryonically, at multiple sites within each bone of

the cranial vault, maxilla, body of the mandible, and midshaft of long bones, mesenchymal cells proliferate and condense.
As vascularity increases at these sites of condensed

mesenchyme, osteoblasts differentiate and begin to produce bone matrix de novo.

It is the replacement of hyaline cartilage with bone and occurs at Ends of all long bones Vertebrae Rib Head of the mandible Base of skull

 Initially mesenchymal condensation occurs.

Chondroblasts are differentiated which then lay down hyaline cartilage.

Mesenchymal cells on the surface of the membrane

form perichondrium which has osteogenic cells.

Hyaline cartilage is formed. This is followed by

formation of perichondrium which has osteogenic cells.

There are 3 zones: zone of proliferation

zone of hypertrophy and maturation zone of provisional

 In early stages type II collagen is laid. Proteoglycans are secreted and there is increase in size. Calcification by alkaline phosphatase and nutrition cut off

leading to cell death and formation of primary areolae .

This is followed by invasion of blood vessels from perichondrium

(primary ossification centre) with osteoblasts (periosteal bud).

Bone development begins at this primary center of ossification

and spreads toward both ends of the cartilaginous model.

 The primary ossification center enlarges proximally

and distally, while osteoclasts break down the newly formed spongy bone and open up a medullary cavity in the center of the shaft.
Around birth, capillaries and osteoblasts will migrate

into the epiphyses and create secondary ossification centers.

 Sutural bone formation is the special case where the

bone forms along sutural margins.

Sutures play an important role in the growing face and

skull. *
Their function is to permit the skull and face to

accommodate growing organs such as the eyes and brain.

 All newly formed bone is cancellous

Osteoblasts line the trabeculae and lay down lamellae Original space retained as the Haversian canal

 The genesis of the alveolar bone is similar to

intramembranous ossification elsewhere in the body.

Trabeculae of woven bone grow and anastomose,

extending from the developing maxillary and mandible, to form the alveolar process.

The alveolar bone of the maxilla develops in mesenchyme.

 In the mandible, the alveolar process develops from

the mesenchyme of the 1st branchial arch, initially adjacent to Meckels cartilage.
The cells responsible for the growth and development

of the alveolar bone are derived from the dental follicle.

The alveolar bone develops around each tooth follicle

during odontogenesis.

 As the 1st tooth buds appear in both maxilla and

mandible, woven bone spicules loosely surround each developing tooth.

The growth of each deciduous and permanent tooth is

accompanied by growth of the trabeculae of alveolar bone.

As the permanent tooth develops, the root of the

deciduous predecessor is progressively resorbed.

 Alongside, the walls of bony crypt and the alveolar

bone, housing the primary tooth, are also resorbed.

With the loss of primary tooth, the succedaneous

tooth moves into the vacated area and new alveolar bone deposited around the eruptive permanent tooth to accommodate its new position and anatomy.
Growth of each permanent molar takes place within its

own separately formed socket.

Characteristics of all bones are outer dense sheet of compact bone and central, medullary cavity. Mature or adult bones are consists of microscopic layers or lamellae. Three distinct types of lamellae are recognized o Circumferential o Concentric o Interstitial

 Circumferential lamellae enclose the entire adult

bone, forming its outer perimeter.

Concentric lamellae make up the bulk of the compact

bone and form the basic metabolic unit of bone; Osteon.

 The osteon is a cylinder of bone, oriented parallel to

the long axis of bone. In the center of each is a canal; Haversian Canal, which is lined by a single layer of bone cells that cover the bone surface, which houses a capillary.
Haversian canals are interconnected by the Volkmann

canals.

Volkmanns Canal
They are canals that run at right angles to the long axis of

the bone.
They contain neurovascular bundles. They connect Haversian canal to central medullary cavity

and surface of the bone.

These canals are not surrounded by concentric lamellae

 Interstitial lamellae are interspersed between

adjacent concentric lamellae and fill the spaces between them.

 Surrounding the outer aspect of every compact bone

is connectve tissue membrane, the periosteum which has two layers: The outer layer of the periosteum is fibrous layer

which consists of a dense, irregular connective tissues.

The inner layer of the periosteum next to the bone

surface consists of bone cells, their precursors and a rich microvascular supply.

 The internal surfaces of compact bone and cancellous

bone are covered by cellular membrane, the endosteum.

It consists of a layer of loose connective tissue with

osteogenic cells that physically separates the bone surface from the marrow within.

 The interdental and interadicular septa contain the

perforating canals of Zuckerkandl and Hirschfeld, which houses the interdental and interadicualr, vessels, lymph vessels and nerves.

 Woven bone (Phase I bone) It plays principal role in healing. It forms quickly (approx 30-60mm/day) but is disorganized

i.e. without lamellar architecture or Haversian system.

It is soft with little biomechanical strength and does not

last long.
It can become highly mineralized when compared to

lamellar bone

 Composite bone

It is a transitional state between woven and lamellar bone. It is a woven bone lattice filled with lamellar bone

 Lamellar bone
It is the most abundant, mature, load bearing,

extremely strong type of bone.

It forms slowly (approx 0.6-1mm/day). It is well organized collagen protein and mineralized

structure. It has multiple oriented layers

 Bundle bone
This is the term given to bone adjacent to the

periodontal ligament that contains greater number of Sharpeys fibres.

It allows for insertion of ligaments and tendons and

consists of striated interconnections with ligaments.

The functional bundle bone is 100-200m

(Habbes 1961).

 Sharpys fibres are principal fibres of periodontal ligament;

also called as extrinsic fibres secreted by periodontal fibroblasts.

angles to the sharpys fibres.

There are also intrinsic fibres which arranged at right

Thus there is double fibrillar orientation. The bundle bone contains fewer fibrils than does

lamellated bone and therefore appears dark in routine H & E stained sections and much lighter in silver stained preparations.

 The tooth is constantly making minor movements and

the bone of socket wall must constantly adapt to the forms of stress. The plasticity of bundle bone is reflected in varying forms of sharpys fibre attachments. They are as follows:Savered Fibres Adhesive Fibres Arborized Fibres Continuous Fibres.

Two cell lineages are present in bone. Osteogenic cells Osteoclasts.

 Origin of bone forming cells :- Mesenchyme

Origin of osteoclasts :- Hematopoietic

For mesenchymal cell to convert into osteoblast, there are two important transcription factors: CBFA-1 (Induced by BMP family) Osx The deletion of each transciption factor results in the lack of bone formation.

Stromal cells in marrow support the differentiation and maturation of hematopioetic cells and maturation of osteoclasts via secreted molecules and via direct cell to cell interaction.

 Mononucleated cells Synthesize collagenous and non collagenous bone

matrix proteins. They arise from pluripotent stem cells which are of ectomesenchymal origin in head. Both preosteoblasts and osteoblasts exhibit high levels of alkaline phosphatase on the outer surface of their plasma membrane. This enzyme is used as a cytochemical marker to distinguish preosteoblast from fibroblast.

The enzyme is believed to cleave organically bound phosphate. The liberated phosphate either: Contributes to the initiation and progressive growth of

bone mineral crystals in hydroxyapatite, or Stimulates the production or maturation of bone matrix itself.
A third possible function, entering the cell and

providing maximal phosphorylation of the several phospho proteins of bone, remains largely untested.

 Osteoblasts are plump cuboidal cells(active) or slightly

flattened cells; that are responsible for the production of organic matrix of the bone. The major constituents of this matrix are type I and type V collagen and small amount of proteoglycans and non collagenous proteins. They exhibit abundant and well developed protein synthetic organelles. The collagen type I is formed within the Golgi complex.

The typical elongated, electron dense, collagen containing secretory granules release their content primarily along the surface of the cell apposed to forming bone. These molecules assemble extracellularly as fibrils to form the osteoid layer.

Noncollagenous proteins are also released mainly along the surface of osteoblasts apposed to osteoid and diffuse from the osteoblast surface towards the mineralization front where they regulate the mineral deposition. Near the mineralizaion front, mineralization foci can be seen within osteoid and certain noncollagenous proteins such as bone sialoprotein, osteopontin are also seen.

In addition to structural matrix proteins, osteoblasts secrete:BMP-2 BMP-7 Transforming Growth Factor b IGF-I and IGF-II PDGF FGF

Osteoblasts form a cell layer over the forming bone surface and have been proposed to act as a barrier that controls ion flux into and out bone. They have been found to have gap junctions that connect them with neighbouring osteoblasts and adjacent bone lining cells, providing an important mechanism for intercellular communication.

When bone is no longer forming, osteoblasts flatten substantially exdending along the bone surface, these cells are known as bone lining cells. Bone lining cells cover most surfaces in adult skeleton.

 As osteoblasts form bone, some become entrapped

within the matrix they secrete, whether mineralized or unmineralized; these cells are then called osteocytes.
The more rapid is the bone formation; the more

osteocytes are present per unit volume.

Embryonic (woven) bone and repair bone have more

osteocytes than the lamellar bone.

 After their formation, osteocytes become reduced in

size. The space in the matrix occupied by osteocyte is known as osteocytic lacuna.
Narrow extentions of these lacunae form canaliculi

through which osteocytes maintain contact with adjacent osteocytes, osteoblasts or bone lining cells.

 This places osteocytes in ideal position to respond

themselves or to transfer signals that affect the response of the other cells involved in bone remodelling to maintain bone integrity and vitality perticularly for the repair of microcracks.
Failure of any part of this interconnecting system

results in hypermineralization (Sclerosis) and death of the bone.

 Larger, multinucleated cells, seen in cluster.

Terminally differentiated and do not proliferate.

Possess TRAP* which distinguishes it from

multinucleated giant cells.

 They are fragile due to their large size*. Highly motile cell that attaches to and move along the

interface between bone and bone marrow i.e. endosteum.

When activated, it attaches to the mineralized bone

matrix and forms a ring like zone of adhesion called sealing zone with the help of osteopontin

 Osteoclasts are found against the bone surface,

occupying hollowed-out depressions called howships lacunae that they have created.
Howships lacunae are shallow troughs with an

irregular shape, reflecting the activity and the mobility of osteoclasts during active resorption.
Adjacent to the tissue surface the osteoclast cell

membrane is thrown into myriad of deep folds that form a ruffled border.

 The space contained inside the ring of attachment+

osteoclasts and the bone matrix constitutes the bone resorbing compartment.
After resorbing to a certain depth, osteoclast detaches

and moves along the bone surface before reattaching and forming another resorption pit.
In the adjacent cytoplasm, next to sealing zone, an

organelle free area is found; known as clear zone.

Tencate described the sequence of events in the

resorption as follows:-

Attachment of osteoclasts to mineralized surface of bone

Creation of a sealed acidic environment through the action of proton pump which demineralizes bone and exposes organic matrix.

Degradation of the exposed matrix by the action of released enzymes

Endocytosis at the ruffled border of inorganic and organic bone degradation products.

Translocation of degradation products in transport vesicles and extracellular release along the membrane opposite the ruffled border.

 Comprises 80-90% of the organic component in

mineralized bone tissues. Type I is the principal collagen. Type I and type V collagen together form heterotypic fibre bundles that provide the basic structural integrity to connective tissues. Type III collagen is present as mixed fibre with type I collagen- in Sharpys fibres. (Huang et al 1991) The collagen fibrils are stabilized by intermolecular cross linking involving lysine and modified lysines that form ring structure

 These cross links are responsible for the high

tensile strength of the collagen fibres.

In woven bone, the fibres are extensively

interwoven, leaving a substantial volume of interfibrillar space that is largely occupied by mineral crystals and acidic proteins.
In mature (lamellar) bone, the collagen fibres form

highly organized sheets in which successive layers of fibres are oriented perpendicular to each other with little interfibrillar space.

Osteocalcin( Bone gla protein)

Produced by osteoblasts; extracellular mineral binding

protein. (Hauschka et al 1989) Represents <15% of non collagenous proteins. Precise function is unclear. However, it indicates role in bone formation. (Bosky 1992) However, osteocalcin binds to osteopontin that interacts with osteoclasts; therefore, it maybe involved in recruiting osteoclasts to sites of newly formed bone; functioning as negative regulator. ( Desbois and Karsenty 1995)

 A glycosylated phosphoprotein.

A potent inhibitor of hydroxyapatite crystal growth.

Mediates the attachment of osteoclasts at all cell-

matrix interfaces. Present at mineralization fronts and cement lines when bone formation follows resorption.

 Comprises 25% of non collagenous proteins.

Ca binding glycoprotein.
Cultural shock glycoprotein. Promotes mineralization of collagen.

Anti adhesive and an inhibitor of cell spreading.

 The alveolar bone proper is seen radiographically as

the lamina dura a thin radioopaque line around the root. The term lamina dura means hard plate and it was used because it looks more calcified.* The spongiosa of alveolar bone can be classified radiographically as:

A. Interdental and interadicular trabeculae are regular and horizontal in ladder like fashion. More common in mandible.
B. Irregularly arranged, numerous, delicate interdental and interradicular trabeculae. Seen in maxilla

 In the embryo and newborn, the cavities of all bones

are occupied by red hematopoietic or yellow inactive marrow.

At birth, all bone marrow is red. With age, more and

more of it is converted to the yellow type.

The hematopoietic compartment of bone marrow

produces approximately 500 billion blood cells per day

 Bone modeling

The process associated with the formation and growth of bones in childhood and adolescence. It consists of processes at the periosteum and endosteum leading to changes in the shape of growing bone.
Bone remodelling

Remove portion of old bone and replace with new one throughtout life. Controlled by local microenvironment

 It was given by German Anatomist/Surgeon Julius

Wolff (1868) Every change in the form or function of bone is accompanied by an adaptive change in the internal architecture and external shape

Stimulating Factors Growth hormone Calcitonin Insulin Testosterone Estrogen Insulin like growth factor TGF Skeletal growth factor BMP PDGF

Inhibiting Factors Cortisol

Stimulating Factors Calcitonin Insulin Vit D

Inhibiting Factors Cortisol

Stimulating factors Parathormone Thyroxine Cortisol Prostaglandins Interleukin-1 Estrogen Calcitonin

Inhbiting factors Cortisol

 Produced by osteoblasts. But most probably derived

from serum and platelets. It is a potent mitogen initiating cell division and a chemotactic factor for cells of mesenchymal origin PDGF stimulates DNA synthesis and cell replication in osteoblasts. Also increases bone collagen synthesis and rate of bone matrix apposition. Principal wound healing hormone.

 Appears to be the principal growth regulator in bone

and cartilage. Act as either paracrine or autocrine regulator of bone formation. Both forms of IGF increase preosteoblastic cell replication and have a stimulatory effect on osteoblastic collagen synthesis and bone matrix apposition and decrease the degradation of collagen. Plays major role in maintaining bone mass.

 One of the most abundant growth factors in bone

matrix. Synthesized by osteoblasts in inactive form. It promotes proliferation and differentiation of mesenchymal precursors for osteoblasts, osteoclasts and chondrocytes. It stimulate type I collagen synthesis.

 It is secreted by parafollicular cells or thyroid gland.

It reduces blood calcium level by decreasing

resorption. It suppresses activity of osteoclasts . It also inhibits development of new osteoclasts

 It consists of 20 proteins.

BMP1 is metalloprotease and remaining belong to

TGF. It is stored in matrix and released during remodelling. BMP 2 and 7 cause osteoblast differentiation. BMP-1 is an enzyme that cleaves the carboxy termini of procollagens I, II and III.

 It stimulates production & release of PGE2 , stimulates

resorption. It has a direct effect on osteoclasts. Stimulates proliferation of osteoclast precursor. It acts indirectly on mature cells to stimulate bone resorption.

 It is secreted by the parathyroid glands.

It increases blood Calcium level by mobilizing calcium

from bone. It decreases excretion of calcium through kidneys. It increases calcium absorption from GI. Also increases phosphate absorption by bone

 The active form is 1,25 dihydroxy cholecalciferol .

It increases blood calcium level by increasing

absorption form small intestine (increases Ca-binding protein expression). It also increases synthesis of alkaline phosphatase in intestine

The most important hormones in bone metabolism are parathyroid hormone, 1,25-dihydroxyvitamin D, calcitonin, estrogen and the glucocorticoids. The hormones affecting bone work primarily through altering the secretion of previously maintained cytokines. The osteoblasts and the lining cells also have anabolic functions and participate in matrix degradation via the production of hydrolytic enzyme and interleukin-6 (IL-6)

It is the method by which bone changes in shape, resistant to forces, repair of wounds and calcium and phosphate homeostasis in body.*

Decrease in Ca level is mediated by receptors on the chief cells of parathyroid glands, which then releases PTH.

PTH stimulates osteoblasts to secrete IL-1 and IL-6 which stimulate monocyte to migrate to bone area. Also LIF coalesce monocytes into multinucleated osteoclasts- resorb bone. This is resorption phase.
Actively resorbing osteoclasts adhere to the bone

surface and produce lacunar pits called Howship's lacunae

A feedback mechanism of normal blood calcium level turns off the PTH secretion. The osteoclasts, meanwhile, have resorbed organic matrix along with hydroxyapetite. The breakdown of collagen from the organic matrix releases various osteogenic substrates. This stimulates the differentiation of osteoblasts, which ultimately deposits bone. This is formation phase. This interdependency of osteoblasts and osteoclasts is known as coupling.

As the osteoclasts move through bone, the leading edge of the resorption is known as cutting cone. When a portion of earlier osteon is left unresorbed, it becomes an interstitial lamella. Behind the cutting cone is a migration of mononucleated cells which they differentiate into osteoblasts and they produce a coating termed as cement or reversal line.* On top of the cement line, osteoblasts lay down new bone matrix, mineralizing it from outside in. The entire area of osteon, where formation occurs, is known as filling cone.

The alveolar bone movement is directed mesioocclusally. At the alveolar fundus, the continuous deposition of bone can be recognized by resting lines. When bundle bone reaches a certain thickness, it is resorbed partly from the marrow spaces and then replaced by lamellated bone or spongy trabeculae. The presence of bundle bone indicates the level at which the alveolar fundus was previously situated.

 Mesial migration of teeth, orthodontic teeth

movement and changes in teeth position during mastication.. All these create region of pressure and tension. Bone surface subjected to pressure reacts by bone resorption while bone subjected to tension exhibit deposition. Usually at the periostal surface, bone formation exceeds bone resorption. And at endosteum surface, modeling leads to greater resorption than bone formation. This results in net expansion of marrow cavity with age.

 Stage of hematoma formation

Stage of granulation tissue

Stage of repair/callus Stage of consolidation

Stage of remodelling

 Rate of 30%-100% is common in growing children.

The rate slows when the adulthood is reached.

About 0.7% of human skeleton resorbed and

replaced by bone everyday Cortical bone turnover rate- 5% per year Cancellous bone & endosteal surface of cortical bone 15% turnover rate per year Normal turnover is 142 days

 Osteophyllic phase
Osteoconductive phase Osteoadaptive phase

Osteophyllic phase
Blood between bone and implant Small amount of bone present Release of cytokines collagen synthesis, regulating

bone metabolism Day 3:- vascular ingrowth End of 1st week:- immune cells By week 1:- ossification. Migration of osteoblasts from endosteum in response to BMP Lasts for 1 month

Osteoconductive phase Lasts for next 3 months peaking between 3-4 weeks Osteoid deposition along metal surface Converted to thin layer of woven bone foot plate(basis stapedis) Fibrocartilagenous callus bone callus (similar to endochondral ossification) 4 months:- maximum surface covered by bone. Steady state. No further bone deposited

Osteoadaptive phase
Balanced remodelling sequence continues Once loaded implants do not gain or lose bone

contact Foot plates thicken

Genetic diseases Osteogenesis imperfecta Osteopetrosis Infantile cortical hyperostosis Marfan syndrome Metabolic bone diseases Rickets Hyperparathyroidism Unknown origin Pagets disease Fibrous displasia

 Because of a deficiency of Type-I collagen.

Extreme fragility of bone and proneness to fracture

Pale blue sclera, deafness Abnormal shape of skull and laxity of ligaments

 Bone becomes sclerotic dense and fragile

Abnormal osteoclastic activity

Bones lack bone marrow Compression of nerves

Anemia due to lack of medullary cavity

 A self-limited inflammatory disorder of infants;

characterized by-Soft-tissue swelling, -Bone lesions -Irritability The cause is unknown.

It is a hereditary disease of autosomal dominant trait. Defective organization of collagen,thus collagen is extremely soluble (less stable intermolecular cross linkage) Clinical features: Disproportionately long and thin extremities. Arachnodactyly or spidery fingers. Skull is disproportionately long Hyperextensibility of joints(dislocation) Myopia CVS complications(cadiomegaly, valve defect).

Oral manifestation:
Highly arched palatal vault.
Bifid uvula. Multiple odontogenic cysts TMJ dysarthrosis.

 Deficiency of Vit. D Impaired metabolism of calcium and phosphorus

Clinical features Craniotabes Pigeon chest Rachitic rosary Bow legs Delayed eruption of teeth Deficiency in adults causes osteomalacia softening of bones

 Excessive secretion of parathormone

Primary:- hyperplasia or adenoma of parathyroid

glands Secondary:- renal dysfunction hyperplasia of parathyroid glands Bone fractures are common Cyst like spaces in jaw (Von recklinghausens disease of bone/osteitis fibrosa cystica)hemosiderin pigment

 Hereditary

Deficiency of alkaline phosphatase

Hypercalcemia Spontaneous fractures

Alveolar bone loss

 Increased risk of fracture

BMD is reduced

Loss of bone matrix and minerals Excess resorption, decrease formation

Architectural deterioration, loss of strength

Commonly affected are vertebrae and hip Treated by bisphosphonates, vit. D

 Isolated areas in which the root is denuded of bone

and the root surface is covered only by periosteum, then overlying gingiva is termed as fenestration. When denuded areas extend through the marginal bone, the defect is called dehiscence. Occurs in approximately 20% of teeth More on facial bone More common in anterior teeth and frequently bilateral.