ALVEOLAR BONE

Alveolar process is the portion of the maxilla & mandible that forms & supports the tooth sockets (alveoli). It forms when the tooth erupts to provide the osseous attachment to the forming periodontal ligament & disappear gradually after the teeth is lost. The alveolar process consists of the followingA. An external plate of cortical bone formed by haversian bone & compact bone lamellae. B. The inner socket wall of thin, compact bone called alveolar bone proper, seen as the lamina dura in radiographs. Histologically, it contains a series of openings (cribriform plate) through which neurovascular bundles link the periodontal ligament. C. Cancellous trabeculae, b/w these 2 compact layers, which acts as supporting alveolar bone. The interdental septum consists of the Cancellous supporting bone enclosed within a compact border.

CELLS & INTERCELLULAR MATRIX

OSTEOBLASTS: The cells that produce the organic matrix of bone, are differentiated from pluripotent cells. Alveolar bone is formed during fetal growth by intramembranous ossification & consists of calcified matrix with osteocytes enclosed within space called lacunae The osteocytes extend processes into canaliculi that radiate from the lacunae. The canaliculi form anastomosing system which brings oxygen & nutrients to the osteocytes through the blood & removes metabolic waste products

 Haversian

system

(oeteons)

are

the

internal

mechanism that bring vascular supply to bones too thick to be supplied only by surface vessels.

BONE

2/3rd of inorganic matter organic matrix

1/3 rd of

Inorganic matter
Mineral calcium & phosphate along with Hydroxyl, Carbonate, Citrate Ions in the form of sodium, magnesium & fluorine Mineral salts are in the form of hydroxyapatite crstals

Organic matrix
Collagen type 1 Non collagenous bone protein; osteocalcin &

osteonectin, sialoprotein

morphogenetic

protein,

phosphoprotein, proteoglycans, osteopontin, bone

 Paracrine factors;cytokines, chemokines, growth factors

REMODELLING
Definition; remodelling is the major pathway of bony changes in shape, resistance to force, repair of wound& calcium & phosphate homeostasis in the body Bone remodelling involves the coordination of activities of cells from two distinct lineage, the osteoblasts & the osteoclasts, which form & resorb the mineralzsed connective tissue of the bone. Regulation of bone remodelling is a complex process involving hormones & local factors acting in an autocrine & paracrine manner on the generation & activity of differentiated bone cells A decrease in blood calcium is mediated by receptor on the chief cells of the parathyroid gland

Release of parathyroid hormones

PTH stimulate osteoblast to release interleukin-1 & interleukin-6 Stimulation of monocyte to migrate into the bone area

Leukemia inhibiting factor(LIF), secreted by osteoblast

Coalesces monocyte into multinucleated osteoclasts Resorption of bone, releasing calcium ions from

hydroxyapatite into the blood

Osteoclasts have resorbed organic matrix along with hydroxyapatite

The

breakdown various

of

collagen

from

organic

matrix are

releases

osteogenic

substrate,

which

covalently bound to collagen, which in turn stimulates the differentiation of osteoblasts which ultimately deposit bone. This interdependency osteoblasts & osteoclasts in remodelling called as coupling

BONE RESORPTION
It is complex process of appearance of eroded bone surface & large multinucleated cells. Osteoclasts originate from hematopoietic tissue Sequence of events in resorptive process as follows1 Attachment of osteoclasts to the mineralized surface of bone. 2 Creation of a sealed acidic environment through action of the proton pump, which demineralise bone & exposes the organic matrix. 3 Degradation of the exposed organic matrix to its constituent amino acids by the action of released enzyme such as phosphatase & cathepsin. 4 Sequestering of mineral ions & amino acids within the osteoclast.

SOCKET WALL
The socket wall consists of dense, lamellated bone, some of which are arranged in haversian systems & bundle bone

BUNDLE BONE is the term given to bone adjacent to the periodontal ligament thet contain a great number of sharpeys fibers It is characterized by thin lamellae arranged in layer parallel to the root, with intervening appositional lines. Bundle bone is localised within the alveolar bone proper. Some sharpeys fibers are completely calcified but most contain an uncalcified central core within a calcified outer layer. Bundle bone occurs throughout the skeletal system wherever ligaments & muscles are attached. Cancellous portion of alveolar bone consists of trabeculae that enclose irregularly shaped marrow space lined with a layer of thin, flattened endosteal cells. Cancellous bone & is found predominantly spaces & in in the

interradicular

interdental

limited

amounts facially or lingually; except in palate. In adult human, more cancellous bone exists in the maxilla than in the mandible.

BONE MARROW

In the embryo & new born the cavities of all bones are occupied by red hematopoietic marrow. The red bone marrow gradually undergoes a

physiologic change to the fatty or yellow inactive type of marrow. Red marrow is found only in the ribs, sternum, vertebrae, skull & humerus

PERIOSTEUM & ENDOSTEUM

The tissue covering the outer surface of the bone is termed periosteum, whereas the tissue lining the interdental bone cavities is called endosteum. The periosteum consists of an inner layer, composed of osteoblasts surrounded by osteoprogenitor cells, which have the potential to differentiate into osteoblasts, & an outer layer rich in blood vessels & nerver & composed of collagen fibers & fibroblasts. The tissue. Inner layer is osteogenic layer, & the outer layer is fibrous layer. endosteum is composed of a single layer of

osteoblast & sometimes a small amount of connective

INTERDENTAL SEPTUM
It consists of Cancellous bone bordered by the socket wall cribriform plates (lamina dura or alveolar bone proper) of approximating teeth & the facial and lingual cortical plate. if the interdental space is narrow, the septum may be consists of only the cribriform plate. B/w maxillary molars, the septum consists of cribriform plate & Cancellous bone in 66.6% of cases. mesiodistal & faciolingual dimensions & shape of interdental septum are governed by the size & convexity of the crown.

OSSEOUS TOPOGRAPHY
The bone contour normally conforms TO the prominence of the roots, with intervening vertical depression that taper toward the margin. The height & thickness of the facial & lingual bony plates are affected by the alignment of the teeth, angulation of root to the bone & occlusal forces. On teeth in labial version, the margin of the labial bone is located farther apically than on teeth in proper alignment.

On teeth in lingual version, the facial bony plate is thicker than normal.

FENESTRATION & DEHISCENCE

The root is denuded of bone & the root surface is covered only by periosteum & overlying gingival are termed fenestrations. Marginal bone is intact When the denuded areas extend through the marginal bone, the defect is called dehiscence. It occurs more common on the facial bone than lingual; anterior than posteriors and are frequently bilateral. Occurs on approximately 20% of teeth

BONE LOSS AND PATTERNS OF BONE DESTRUCTION

Bone destruction caused by extension of gingival inflammation The most common cause of bone destruction in periodontal disease is the extension of inflammation from the marginal gingival into the supporting periodontal tissue. Periodontitis is always preceded by gingivitis, but not all gingivitis progresses to periodontitis The transition from gingivitis to periodontitis is associated with changes in the composition of bacterial plaque The cellular composition of infiltrated connective tissue also changes with increasing severity of the lesion Fibroblasts and lymphocytes predominate in stage 1 gingivitis, whereas the number of plasma cells and blast cells increases gradually as the disease progresses.

 The extension of inflammation to structures of a tooth may be pathogenic potential of plaque

supporting modified by

RATE OF BONE LOSS

Loss to average about 0.2 mm a year for facial surface and about 0.3 mm a year for proximal surfaces when periodontal disease was allowed to progress untreated. Based on interproximal loss of attachment and tooth mortality described Approx. 8% of persons had rapid progression of periodontal disease, characterized by a yearly loss of attachment of 0.1mm to 1.0mm following 3 sub groups has been

 Approx. 81% of individual had moderately progressive periodontal disease, with a yearly loss of attachment of 0.05mm to 0.5mm The remaining 11% of persons had minimal or no progression of destructive disease (0.05mm-0.09mm yearly)

PERIODS OF DESTRUCTION
The destructive periods result in loss of collagen & alveolar bone with deepening pocket . Following theories are given ; Bursts of destructive activitiy are of the periodontal

associated with subgingival ulceration and an acute inflammatory reaction, resulting in rapid loss of alveolar bon Bursts of destructive activity coincide with the conversion of a predominantly Tlymphocyte infiltrate Periods of exacerbation are associated with an increase of the loose, unattached, motile, gram-negative anaerobic pocket lesion to one with a predominantly B- lymphocyte plasma cell

flora & periods of remission coincide with the formation of a dense, unattached, non-motile, gram-positive flora with a tendency to mineralize. Tissue invasion by one or several bacterial species is followed by an advanced local host defence that controls the attack

MECHANISM OF BONE DESTRUCTION Bacterial plaque products induce the differentiation of bone progenitor cells into osteoclasts & stimulate gingival cells to release mediator.

Plaque products & inflammatory mediator can also act directly on their numbers.

Host factors released by inflammatory cells are capable of inducing bone resorption in vitro & can play a role in periodontal disease. (these includes host- produced prostaglandins & their precursors, interleukin- 1 (1L-1) & 1L- and tumor necrosis factor(TNF-)

BONE DISEASE

FORMATION

IN

PERIODONTAL

Area of bone formation are also found immediately adjacent to sites of active bone resorption & along trabecular surfaces at a distance from the inflammation, in an apparent effort to reinforce the remaining bone. The response of alveolar bone to inflammation includes bone formation & resorption; thus, bone loss in periodontal disease is not simply a destructive process but results from the predominance of resorption over formation

BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION

Another cause of bone destruction is trauma from occlusion, which can produce bone destruction in the absence or presence of inflammation. In the absence of inflammation, the changes caused by trauma from occlusion vary from increased compression & tension of the periodontal ligament & increased osteoclasts of alveolar bone to necrosis of

periodontal ligament & bone and resorption of bone & tooth structure Persistent trauma from occlusion result in funnel shaped bone widening of the crestal portion of the periodontal ligament, with the resorption of adjacent

BONE DESTRUCTION CAUSED BY SYSTEMIC DISORDERS

Local & systemic factors regulate the physiologic equilibrium of bone. When a generalised tendency toward bone resorption exists, bone loss initiated by local inflammatory processes may be magnified The amount & virulence of plaque bacteria,the nature of the systemic component, not its presence or absenc , influences the severity of periodontal destruction Osteoporosis is a physiologic condition of post

menopausal women,

resulting in the loss of bone

mineral content & structural bone changes Periodontal bone loss may also occur in generalised skeletal disturbances (e.g hyperparathyroidism, leukemia, langerhans cell histiocytosis) by mechanism.

FACTORS MORPHOLOGY DISEASE

DETERMINING IN

BONE

PERIODONTAL

Normal variation in alveolar bone

 The thickness, width and crestal angulation of interdental septa The thickness of the facial & lingual alveolar bone The presence of fenestrations & dehiscences The alignment of the teeth Root & root trunk anatomy Root position within the alveolar process Proximity with another tooth surface Exostoses Outgrowth of bone of varied size & shape. They can

occur as small ,nodules, large nodules, sharp nodules, sharp ridges and spike like projections

Trauma from occlusion

It may cause a thickening of cervical margin of alveolar bone or change in morphology of bone e.g angular defects Buttressing bone formation (lipping) Bone formation sometimes occurs in an attempt to buttress bony trabeculae weakened by resorption. When it occurs within the jaw, it is termed central buttressing bone formation. When it occurs on external surface, it is referred to as peripheral bone formation

Food impaction

Interdental bone defects often occur where proximal contact is absent or abnormal The poor proximal relationship may result from a shift in tooth position because of extensive bone destruction preceding food impaction Aggressive Periodontitis A vertical or angular pattern of alveolar bone

destruction is found around the 1st molars in aggressive Periodontitis

BONE

DESTRUCTION

PATTERN

IN

PERIODONTAL DISEASE
Horizontal bone loss It is most common pattern of bone loss in periodontal disease, the bone is reduced in height, but the bone margin remains approx. perpendicular to the tooth surface Vertical or angular defects These defects are those that occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root; the base of the defect is located apical to the surrounding bone

Angular defects are classified on the basis of the no. of osseous walls Angular defects may have one, two or three walls The no. Of walls in the apical portion of defect may be greater than that in its occlusal portion, it is termed as combined osseous defect Vertical defects occurring be seen on the radiographs Angular defects can also appear on facial & lingual or palatal surface, but not seen in radiographs Vertical defects increase with age The three wall defect was originally called an intrabony defect, this appears most frequently on mesial aspect of 2nd & 3rd maxillary & mandibular molar One wall vertical defect is also called hemiseptum interdentally can generally

Osseous craters

Osseous concavities in the crest of the interdental bone confined within the facial & lingual walls The following reason for the high frequency of

interdental craters The interdental area collects plaque & difficult to clean The normal flat or even concave faciolingual shape of the interdental septum in lower molar may favour crater formation Vascular pattern from the gingival to the center of the crest may provide a pathway for inflammation

Bulbous bone contours They are bony enlargements caused by exostoses, adaptation to function or buttressing bone formation. More in maxilla than mandible

Reversed architecture They are produced by loss of interdental bone,

including the facial plates & lingual plates, without concomitant loss of radicular bone Most common in maxilla

Ledges Ledges are plateau like bone margins caused by resorption of thickened bony plates

furcation involvement It refers to the invasion of the bifurcation & trifurcation of multirooted teeth by periodontal disease grade 1; is incipient bone loss grade 2; partial bone loss (cul-de-sac) garde 3; total bone loss with through and through opening of furcation grade 4 ; gingival recession exposing the furcation

References Carranza ;bone loss & patterns of bone destruction Carranza;Alveolar bone

CONTENTS
Definition Cells & intercellular matrix Remodelling Bone resorption Socket wall Bone marrow Interdental septum Osseous topography Fenestration & dehiscence Bone loss and pattern of bone destruction Rate of bone loss Periods of destruction Mechanism of bone destruction Bone formation in periodontal disease Bone destruction caused by trauma Bone destruction caused by systemic disorders Factors determining bone morphology in periodontal disease Bone destruction pattern in periodontal disease References