BONE LOSS AND PATTERNS OF BONE DESTRUCTION

Bone:- is a specialized mineralized connective
tissue. The basic functions of bone are: 1. Support 2. Protection 3. Movement 4. Mineral homeostasis 5. Site of blood cell production 6. Storage of energy

Composition of bone:
BONE inorganic 67% Hydroxyapatite organic 33% Collagen 28% 5% Oesteocalcin Sialoprotein Phosphoprotein Osteonectin Bone specific protein

BONE CELLS:- Bone is composed of cells embedded in a stiff calcified matrix. 1. Osteoprogenitor stromal cells 2. Osteocytes 3. Bone lining cells. 1. Osteoprogenitor stromal cells :- These are derived from pluripotent stromal stem cells present in the bone marrow and other connective tissues which can proliferate and differentiate into osteoblasts prior to bone formation. The two types of osteoprogenitor cells are 1. Totally committed to bone formation 2. Inducible osteoprogenitors present in the connective tissues.

BONE LINING CELLS:These are flattened cells seen in the adult skeleton which are found on the resting surface of the bone. They form a continuous layer and are in contact with each other. They are present on the periosteal surface and line the system of vascular canals with osteoid. OSTEOBLAST:It is a uninucleated cell that synthesizes both collagenous and non collagenous bone proteins and is responsible for its mineralisation. It forms a cellular layer on the bone surface. Osteoblasts exhibit high levels of alkaline phosphatase. Under the light microscope, it appears as a plump cell with open faced nucleus and abundant basophilic cytoplasm.

OSTEOCYTES :As osteoblasts secrete bone matrix some of them become entrapped in the lacunae and are called osteocytes. After formation, osteocytes gradually lose most of their matrix synthesizing machinery and becomes reduced in size. The most important function of osteoblast and osteocyte complex is to prevent hyperminerlization of bone by continually pumping calcium back into the blood stream.

Osteoclast:It is a multinucleated large cell, because of their size they can be easily identified under light microscope. Typically osteoclasts are found against bone surfaces occupying shallow hollowed depressions called Howship¶s lacunae. Generally it is stated that origin of the bone forming cells is from mesenchymal source where as, origin of osteoclast is from haemopoetic tissue.

The inner structure of the bone shows three distinct type of layering 1. Circumferential 2. Concentric 3. Interstitial Circumferential :It encloses the entire adult bone forming its outer perimeter. Concentric:It makes up the bulk of the compact bone. The basic metabolic unit of compact bone is the osteon.

The osteon is a cylinder of bone generally oriented along the long axis of the bone. In the center of each osteon is the haversian canal which is lined by a single layer of bone cells. 3. Interstitial:These are present between the concentric and lamellar bone

STRUCTURE OF MATURE BONE Compact bone is white with a dense texture which is usually limited to the cortices of mature bone. Cancellous bone shows honey combed large cavities with reduced lattice work. The alveolar process is the portion of the maxilla and mandible that forms and supports the tooth socket.

The bone lining the socket is referred to as bundle bone because it provides attachment for the ligament fiber bundles. It is perforated by many foramina which transmits nerves and vessels and hence is referred to as cribriform plate. BUNDLE BONE:- is the term given to bone adjacent to the periodontal ligament that contain a great number of Sharpey¶s fibers. WOVEN BONE:- is the first type of bone to be formed during skeletal development and also the first bone to be laid down during repair.

BONE LOSS AND PATTERNS OF BONE DESTRUCTION
‡ Although periodontitis is an infectious disease of the gingival tissue, the changes that occur in bone are crucial because it is the destruction of the bone that is responsible for tooth loss. ‡ The height of the alveolar bone is normally maintained by an equilibrium regulated by local and systemic influences between bone formation and bone resorption.

‡ When resorption exceeds formation bone height is reduced.

‡ Bone destruction in periodontal disease which are caused by local factors are
A) Those that are caused by gingival inflammation. B) Those that are caused by trauma from occlusion. ‡ Bone loss caused by extension of gingival inflammation is responsible for reduction in the height of the alveolar bone. ‡ Trauma from occlusion causes bone loss lateral to root surface.

‡ Bone destruction caused by extension of gingival inflammation :-

Chronic inflammation is the most common cause of bone destruction in periodontal disease.

The extension of inflammation from the marginal gingiva to the supporting periodontal tissues marks the transition from gingivitis to periodontitis.

‡ This transition is associated with the changes in the composition of bacterial plaque because in the advanced stage of the disease the number of motile organisms and spirochetes increases where as the number of coccoid and straight rods decreases ‡ The cellular composition also changes with the increasing severity of the lesion ‡ A) Fibroblasts and lymphocytes predominate in stage I gingivitis ‡ B) Plasma cells and blast cells increases gradually as the disease progresses

‡ The lesion becomes progressively destructive when it is infiltrated with B lymphocytes ‡ The pathway of spread of inflammation is critical because it affects the pattern of bone destruction in periodontal disease ‡ HISTOPATHOLOGY: Gingival inflammation extends along the collagen fiber bundles, and follows the course of the blood vessels through the loosely arranged tissues around them into the alveolar bone

‡ Inter proximally inflammation spreads in the loose connective tissue around the blood vessels through the transseptal fibers , and then into the bone through the vessel channels that perforate the crest of the inter dental septum. ‡ After reaching the marrow spaces the inflammation may return from bone into the periodontal ligament

‡ Facial and lingual inflammation from gingiva spreads along the outer periosteal surface of the bone and penetrates into the marrow spaces through the vessel channels in the outer cortex. ‡ Along its course from the gingiva to the bone the inflammation destroys the gingiva & the transseptal fibers

‡ After the inflammation reaches the marrow spaces it replaces the marrow with a leukocytic fluid exudate which contains fibroblasts and multinuclear osteoclasts. ‡ The number of mononuclear phagocytes are increased . ‡ The bone surfaces are lined with µcove-like¶ resorption lacunae.

‡ In the marrow spaces, resorption causes thinning of the surrounding bony trabeculae followed by destruction of bone and reduction in bone height ‡ Normally fatty bone marrow is partially or totally replaced by a fibrous type marrow in the vicinity of the resorption ‡ Bone destruction in periodontal disease is not a process of bone necrosis , it involves activity of living cells along the viable bone

‡ The two cell types involved in bone resorption : ‡ A) Osteoclast ± which removes the mineral portion of the bone. ‡ B)Mononuclear cells ± which play a role in organic matrix degradation. ‡ RADIUS OF ACTION :- Page and Schroeder on the basis of Waerhaug¶s measurements postulated that there is a range of effectiveness of about 1.5 to 2.5 mm within which bacterial plaque can induce bone loss

‡ RATE OF BONE LOSS:- Varies depending on the type of the disease present. ‡ Loe & coworkers identified 3 sub groups of patients with periodontal disease based on interproximal loss of attachment and tooth mortality. ‡ 1) 8% of the subjects had rapid progression of periodontal disease characterized by yearly loss of attachment of 0.1 to 1 mm

‡ 2) 81% of the individuals had moderately progressive periodontal disease with yearly loss of attachment of 0.05 to 0.5 mm

‡ 3) 11% of individuals had minimal or no progression of destructive periodontal disease with yearly attachment loss of 0.05 to 0.09 mm

‡ PERIODS OF DESTRUCTION :‡ Periodontal destruction occurs in an episodic, intermittent fashion with alternating periods of inactivity or quiescence and destructive periods resulting in loss of collagen and alveolar bone ‡ It could be due to Bursts or destructive activity associated with subgingival ulceration and an acute inflammatory reaction resulting in rapid bone loss. This coincides with conversion of predominantly T lymphocyte lesion to one with predominance of B lymphocyte

New bone formation retards the rate of bone loss, compensating in some degree for the bone destroyed by inflammation. This indicates that bone resorption in periodontal disease may be an intermittent process with periods of remission & exacerbation. Periods of exacerbation are associated with an increase of a loose unattached, motile gram negative anaerobic pocket flora . Periods of remission show formation of dense unattached non motile gram +ve flora .

MECHANISM OF BONE RESORPTION
Host and bacterial factors are involved in bone resorption The substances that can induce resorption in periodontal disease comes from two sources 1. Subgingival bacteria 2. Periodontal tissues

BACTERIAL FACTORS a) Lipopolysaccharides from gram ±ve bacteria (Hausmann et al- 1970) b) Lipoteichoic acid from Actinomyces viscosus (Hausmann et al-1974) c) Peptidoglycan(Lens graf et al- 1979) d) Muramyl dipeptide(Dewhirst- 1982)

‡ Some bacterial lipopolysaccharides such as that from E.corrodens also release cytokines such as IL-1 and IL-6 from osteoblasts and fibroblasts. ‡ Lipopolysaccharides are known to activate complement cascade by alternative pathway which in turn generates prostaglandins.

‡ Surface associated material from P.gingivalis and E.corrodens can stimulate production of prostaglandin E2 and collagenase from bone cells (Harvey et al- 1986) ‡ Surface associated material from A .actinomycetomcomitans also causes bone resorption by mimicking action of IL-1

‡ The main cytokine released from connective tissue and bone cell by surface associated material is IL6 . This has been shown to stimulate the formation of osteoclast (Lowick et al- 1989) ‡ The surface associated material from A.actinomycetemcomitans are made up of number of proteins & peptides with potent biological actions that are relevant to the pathology of both chronic and juvenile periodontitis

‡ A)A protein with potent osteolytic activity is called as Chaperonin-60 (Kirby et al1995) ‡ B)A protein with antimitotic activity is called as Gapstatin (White et al - 1995)

HOST FACTORS
‡ The Main host derived bone resorbing factors are:1. Eicosanoids 2. Cytokines I. Eicosanoids:Prostaglandins, Hydroxyeicosatetraenoic acid (HETE) and Leukotrienes are inflammatory mediators derived from cell membrane phopholipids by the action of cyclooxygenase or lipoxygenase on arachidonic acid. These are secreted by macrophages, PMNs and endothelial cells.

‡ (a)The prostaglandin (PG) was the first mediator of local bone resorption to be discovered and the most important are PGE1, PGE2 and prostacyclin (PGI-2) [Deetrich et 1975] but PGE2 is the most potent in causing bone resorption. ‡ The GCF Levels of PGE2 also correlate with the periodontal disease status [Offenbacher et al 1986]

(b) Hydroxyeicosatetraenoic acid stimulates bone resorption (c) Other products of inflammation like heparin from mast cell can enhance bone resorption under the influence of lipopolysaccharides and lipoteichoic acid (d) Thrombin is a potent bone-resorbing agent

CYTOKINES
The Cytokines that have been shown to stimulate bone resorption are:a. IL-1 and 1 [Gowen and Munday 1986] b. TNF and ± [Bertolini et al] c. Transforming growth factors [TGF] d. Platelet derived growth factor (PDGF) [Tashian et al] e. IL ± 6 Leads to osteoclastic activity But the most potent stimulators of bone resorption are IL ± 1 and TNF IL-1 , IL-1 and TNF are found in the GCF

MECHANISM OF BONE RESOPTION: Bone resorption cannot occur without the presence of both osteoblasts and osteoclasts ‡ All systemic and local bone resorbing factors exert their influence by stimulating the osteoblast and this osteoblast is involved in the regulation of osteoclast function at several levels

Osteoblasts have receptors for systemic factors such as parathormone and vitamin D which affects general remodeling, and locally release factors such as prostaglandins and cytokines which affects local changes and exert their influence by stimulating the osteoblasts in a specific way. Osteoblast stimulated by these factors mediate their response through a series of intracellular secondary messenger systems, One pathway involves cyclic AMP and second involves membrane phospholipids and protein kinase.C.

Both these mechanisms are stimulated by PGE2, prostacyclin (PGI2) and thrombin In response to these stimuli osteoblasts secrete factors that prepares the bone surface for osteoclastic resorption and stimulates the development of functional osteoclast Osteoblast stimulates osteoclast formation by the secretion of cytokines and cell to cell contacts

Osteoblasts secrete growth factors like a.Granulocyte macrophage colony stimulating factor and IL-6, which in turn stimulates the differentiation and maturation of the cells into osteoclasts. b. Prostaglandins and proteins made up of two components which are responsible for activation of the mature osteoclast

c.

Stimulated osteoblasts also secrete procollagenase and plasminogen activator which generates plasmin from plasminogen and this activates procollagenase for removing the non mineralised collagenase surface layer. Osteoclastic resorption first involves a solubulization of the mineral phase and secondly dissolution of the organic matrix

d.

The resorption area is defined beneath the ruffled border of the osteoclast. This is a highly specialized region of cytoplasmic infolding of the plasma membrane . This contains podasomes which are specialized protrusions of the ventral membrane of the osteoclast which adhere directly to the bone surface being broken down.
The minerals are dissolved by acid secretion which is brought about by an electrogenic hydrogen ion transporting system. This is an ATP driven proton pump.

Intracellular pH regulation is achieved by carbonic anhydrase which is abundant in the osteoclast cytoplasm. Bicarbonate generated by the carbonic anhydrase appears to be secreted from the basal outer membrane & the hydrogen ions which are released in the functional extracellular lysomal compartmant solubilize the mineral component. Osteoclasts also produce reactive oxygen species (ROS) which may play a role in the pathological demineralization of bone during disease [Garret et al 1990]

The degradation of the demineralised bone matrix involves the secretion of acid cysteine proteinases including cathepsins B,L and N The Degradation of the demineralised organic matrix of bone by osteoclast involves the production, secretion and function of both cysteine and metalloproteinases. by [Evert at al 1994]

MARKERS OF BONE RESORPTION Several bone morphogenic proteins are involved in bone mineralization and some connective tissue proteins also play an important role in this process. Some of them are considered as possible markers of bone resorption and periodontal disease activity.

a. b. c. d. e. f. a.

Osteonectin Bone phosphoprotein Osteocalcin Telopeptides of Type-1 collagen Collagen I Proteoglycans Osteonectin and Bone phosphoprotein Osteonectin is a normal component of bone matrix which plays an important role in the initial phase of mineralization [by Terimine et al 1981]

b. Bone Phosphoprotein is an amino propeptide extension of the alpha 1 chains of type-1 collagen Both these proteins have been detected in GCF from patients with periodontitis (Bowers et al 1989) c. osteocalcin is a 5.4 KD calcium binding protein of bone. osteocalcin also chemotactically attracts osteoclast progenitor cells and blood monocytes. In high concenterations it inhibits collagen synthesis in osteoblasts and promotes bone resorption

Further more,elevated levels of osteocalcin are found in the blood during periods of rapid bone turnovers such as osteoporosis For all these reasons, osteocalcin has been suggested as a possible marker GCF osteocalcin levels reflect the degree of inflammation 4. Telopeptide of type-I Collagen is 12-20 KD fragment of bone.

Type-1 Collagen released by digestion with trypsin or bacterial collagenase and elevated cross-link telopeptide has been shown to coincide with bone resorptive rate CTP levels in GCF are very high in individuals with periodontitis DEVELOPMENT OF DIAGNOSTIC KITS Most of the potential markers could easily be adapted into test kits as their detection involves the use of specific polyclonal and monoclonal antibodies

Advantages 1.Some of these potential markers are associated with disease activity 2.They are simple to use. 3.They can be read after relatively short periods 4.They can be shown to the patient and related to the tooth site affected Disadvantages: 1.The choice of the most appropriate biomarker is difficult with the present state of knowledge 2. There is difficulty in determining the sites to sample 3. Cost.

BONE DESTRUCTION CAUSED BY TRAUMA FROM OCCLUSION Trauma in the absence of inflammation a. Trauma from occlusion leads to increased compression and tension of the periodontal ligament , increased osteoclasis of alveolar bone, necrosis of the periodontal ligament and resorption of bone. b. Persistent trauma from occlusion results in the funnel shaped widening of the crestal portion of the periodontal ligament with resorption of the adjacent bone

Trauma in the absence of inflammation When combined with inflammation, the trauma from occlusion aggravates the bone destruction caused by inflammation and causes bizarre bone patterns. Local and systemic factors regulate the equilibrium of bone. When there is general tendency towards bone resorption, bone loss initiated by local inflammatory process may be magnified.This systemic influence on the response of alveolar bone is termed as Bone Factor in periodontal disease

BONE DESTRUCTION caused by systemic disorders Periodontal bone loss may also occur in generalized skeletal disturbances like, 1. Hyperparathyroidism 2. Leukemia Schuller Christian disease Factors determining bone morphology 1. The thickness, width, and crestal angulation of the interdental septa 2. 3. The thickness of facial and lingual alveolar plates The presence of fenestrations and dehiscence 3. Hand

4. The increased thickness of the alveolar bone margin to accommodate functional demands.

BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE Horizontal bone loss :-This is the most common pattern of bone loss in periodontal disease . The bone is reduced in height, but the margin remains roughly perpendicular to the tooth surface. The interdental septa, facial and lingual plates are affected Bone deformities (Osseous defects):1. Vertical or angular defects :- are those that occur in the oblique direction , leaving a hollowed out trough in the bone along side the root.The base of the defect is located apical to the surrounding bone , and is usually accompanied by infrabony pockets.

Angular defects are classified on the basis of the number of osseous walls.It may be one , two or three walls. The number of walls in the apical portion of the defect may be greater than the occlusal portion. In these cases, the term µcombined osseous defect¶ is used a. Angular defects can also appear on the facial and lingual surfaces but these are not seen on radiographs and surgical exposure is the only way to determine the vertical osseous defect Three wall vertical defect has also been called an µintrabony defect,¶. This defect appears most frequently on the mesial aspects of second and third maxillary and mandibular molars The one wall defect is called µ Hemiseptum¶

Osseous craters :- are the concavities in the crest of the inter dental bone confined within the facial and lingual walls , are more common in the posterior segments The following reasons have been suggested 1. The interdental area plaque is difficult to clean 2. The normal flat or even concave faciolingual shape of the interdental septum in lower molars may favour crater formation 3. Vascular patterns from the gingiva to the center of the crest may provide a pathway for inflammation

Bulbous bone contours: These are bony enlargements caused by exostoses , adaptation to function or buttressing bone formation. They are found more frequently in the maxilla than the mandible Reverse Architecture:- These defects are produced by the loss of interdental bone , including facial and lingual plates without concomitant loss of radicular bone , there by reversing the normal architecture and are more common in the maxilla. Ledges:- are plateau like bony margins caused by resorption of the thickened bony plates.

Furcation Involvemevt :- The term furcation involvement refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease . The denuded furcation may be visible clinically or covered by the wall of the pocket Furcation Involvement has been classified as 1. Grade I:- incipient bone loss 2. Grade II:- partial bone loss (cul de sac) 3. Grade III:- total bone loss with through and through opening of the furcation 4. Grade IV:- is similar to Grade III but gingival recession exposes the furcation.

Furcation involvement is a stage of progressive periodontal disease The etiological factors could be a. Trauma from occlusion should be particularly suspected when crater like or angular deformities in the bone b. Enamel projections in the furcations

c. The presence of accessory pulpal canals in the furcation area may extend the pulpal inflammation to the furcation.

Bone Changes a. Exostoses are outgrowths of bone of varied size and shape.They can occur as small nodules,sharp ridges or spike like projections. b. Buttressing bone formation (Lipping) ± Occurs sometimes in an attempt to buttress bony trabeculae weakened by resorption.When it occurs within the jaw it is called µcentral buttressing bone formation¶.When it occurs in the external surface it is referred as µperipheral buttressing bone formation¶. The latter may cause bulging of the bone contour called µlipping¶.

c. Food Impaction: Interdental bone defects often occur where proximal contact is abnormal or absent. Pressure and irritation from food impaction contribute to the inverted bone architecture. d. Juvenile periodontitis: A vertical or angular pattern of alveolar bone destruction is found around the first molars.

Treatment for Furcation involvement: Grade I: It usually exhibits suprabony pockets which are treated by scaling and curettage .

Grade II: Under L.A each tooth surface is probed down to the bone to determine the pattern of periodontal destruction and treated with osseous repair by variety of a.osseous grafting techniques, a.Guided tissue regeneration methods, c.combination of both

Treatment of choice for Grade III and Grade IV involvements is Flap Surgery, as the success with regenerative procedures with different graft materials and membranes have been very limited. Furcation involvements combined with vertical bone defects require bone contouring as well as instrumentation of the root surface facing the furcation. The treatment of advanced Grade II and Grade III Furcation Involvements will often require removal or resection of the root. The removal of the root without the removal of any portion of the crown is termed as Root Resection or Root Amputation. When one of the root and its corresponding crown is removed it is called Hemisection.

In case of a mandibular molar it can be accomplished by Bisection (Bicuspidization) The morphology of the osseous defect will largely determine the treatment and technique to be used. a. One Wall angular defects usually have to by recontoured surgically. b. Two Wall angular defects can be treated by new attachment and bone regeneration.

c. Three wall angular defects particularly if they are narrow and deep can be successfully treated with new attachment and bone regeneration. The osseous corrective procedures are used to treat shallow craters with heavy faciolingual ledges Exostoses is corrected by resective osseous

surgery.

Patient with advanced periodontal Disease
Initial therapy (scaling and root planning oral hygiene training) Reevaluation (PAL, bleeding on open probing X-ray films)
B A

Plaque index > 15% Surgery not advisable, Continue maintenance

Plaque index < 15%, Minimal bleeding on probing

Assess : Defect topography Infection with suspected Significant periopathogen Horizontal bone loss
D Assess : Remaining pocket depths Pockets < 5mm
RESECTIVE PROCEDURES TISSUE ATTACHMENT PROCEDURES

C

Vertical bone defects or Furcation involvements
E F Infection with Suspected significant periopathogen Use of appropriate antibiotics

Non vital tooth
Endodontic treatment

Class III mobility
Provisional splinting

Pockets > 5mm

Extraction or maintenance

REGENERATIVE PROCEDURES

GTR

Conclusion
The response of alveolar bone to inflammation includes bone formation as well as resorption. Thus bone loss in periodontal disease is not simply a destructive process, but results from the predominance of resorption over formation.

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