INTRODUCTION: The height of the alveolar bone is normally maintained by equilibrium, between bone formation and bone resorption.

When resorption exceeds formation, bone height is reduced. Loss of alveolar bone support is one of the characteristic signs of destructive periodontal disease and is considered to represent the anatomical sequel to the spread of periodontitis. A variety of factors other than the main local factors, plaque, play a role in bone destruction. Acting singly or together, these factors are responsible for bone destruction in periodontal disease and determine its severity and pattern. The level of bone is the consequence of past pathologic experiences, whereas changes in the soft tissue of the pocket wall reflect the present inflammatory condition. Therefore, the degree of bone loss is not necessarily, correlated with the depth of periodontal pockets, the severity of ulceration of the pocket wall, or the presence or absence of pus. Chronic inflammation is the most common cause of bone destruction in periodontal disease, as it results in the extension of the inflammatory process to the bone. The extension of inflammation from the marginal gingiva into the supporting periodontal tissues marks the transition from gingivitis to periodontitis. Various components of host response particularly the cytokines and matrix metalloproteinases (MMPs) are considered to be responsible for the bone loss. In addition, substances produced by the sub-gingival bacterial flora during inflammation and immune reactions may alter bone turnover by either causing the differentiation and stimulation of osteoclasts or by inhibiting bone formation by osteoblasts. Thus, the progression of periodontal disease and amount of bone loss depend upon the host response. The other main cause of periodontal destruction is trauma from occlusion. Bone loss, caused by extension of gingival inflammation is usually found as reduction in the height of the alveolar bone, whereas trauma from occlusion causes bone loss lateral to the root surface.

Though the role of trauma from occlusion in causing bone loss was considered controversial for many years, it is now considered as one of the main co-factors responsible for the progression of periodontal disease and subsequent bone loss. Trauma from occlusion can also cause bone loss in the absence of inflammation. Likewise smoking, stress and various systemic disorders may cause bone loss. The extent and severity of alveolar bone loss are assessed by a combination of radiographic and clinical means. More recently, various computerized methods have been introduced to give a more precise and detailed view of the amount and type of bone loss.

Factors Responsible for Bone Resorption:

Parathyroid Hormone (PTH): It has been known for 70 years that parathyroid hormone (PTH) affects bone cell function, may alter bone remodeling, and cause bone loss. It is now apparent that PTH acts on both bone-resorbing cells and bone-forming cells. The net effect of the hormone depends on whether it is administered continuously or intermittently. When administered continuously, it increases osteoclastic bone resorption and suppresses bone formation. However, when administered in low doses intermittently, its major effect is to stimulate bone formation, a response that has been called the anabolic effect of PTH. PTH stimulates osteoclasts to resorb bone. In organ cultures, PTH increases osteoclast activity, with resultant degradation of bone matrix. PTH activates mature osteoclasts to resorb bone, whereas other agents exert their effects by increasing the formation of new osteoclasts. It stimulates mature, multinucleated osteoclasts to form ruffled borders and resorb bone. However, the precise molecular mechanism by which PTH exerts its effects on these cells is still not known. The effect of PTH on osteoclast precursors is combined with direct effects on the cell itself, with an indirect effect of regulating other cells to produce local factors that influence the osteoclast precursor cells, such as regulating cells of the granulocyte-macrophage type, to produce granulocyte-monocytecolony stimulating factor (GM-CSF). The effect of PTH on mature osteoclasts is also indirect because osteoclasts will not resorb bone unless osteoblasts are present,

suggesting that PTH may stimulate osteoclastic bone resorption by interacting with cells in the osteoblast lineage. The mechanisms used by cells of the osteoblast phenotype to communicate with osteoclasts are still not known. It has been suggested that osteoblasts may prepare the bone surface for osteoclastic bone resorption by producing proteolytic enzymes. However, this theory is still questionable.

1, 25-Dihydroxycholecalciferol (I, 25 (OH) 2 D 3):

The active metabolites of vitamin D3 have complex effects on calcium homeostasis and bone regulation. I, 25 (OH)2 Ds stimulates osteoclastic bone resorption in vitro and in vivo. The active metabolites of vitamin D3 have complex effects on calcium homeostasis and bone regulation. I, 25 (OH)2 D3 stimulates osteoclastic bone resorption in vitro and in vivo. It has a very slow onset of action, with a shallow dose-response curve. It increases both osteoclast number and activity, with an increase in ruffled border size and clear-zone volume. Mature osteoclasts do not have receptor for I, 25 (OH)2 D3 which increases both osteoclast number and activity, with an increase in ruffled border size and clear-zone volume. Mature osteoclasts do not have receptors for I, 25 (OH)2 D3. Thus, the effects of this hormone on mature osteoclasts are most likely mediated indirectly through other cells. The major effect of I, 25 (OH)2 D3 on osteoclastic bone resorption may be to stimulate the fusion of differentiation of committed osteoclast progenitors to form mature cells. Use of I, 25 (OH)2 D3 influences and modulates cytokine production by immune cells.

Calcitonin:
Calcitonin has been demonstrated to inhibit osteoclastic bone resorption. The effect of calcitonin on osteoclasts is mediated through cyclic AMP. Calcitonin decreases osteoclast activity. The effects of calcitonin on bone resorption are short-lived; however, osteoclasts eventually lose their responsiveness to calcitonin after continuous exposure, a phenomenon referred to as escape.

One explanation for this phenomenon may involve a decrease in receptor number after long periods of exposure. Another possible explanation is that, a second population of osteoclasts, which is not responsive to calcitonin, emerges. It is believed that it inhibits bone resorption transiently when bone turnover is not needed for calcium homeostasis.

Estrogens:
Estrogen clearly inhibits the increase in bone resorption associated with menopause. Following estrogen withdrawal, an initial increase in bone turnover can be observed. Later, bone resorption occurs faster than bone formation, with a net effect of bone loss. The effects of estrogen are mediated by a combination of direct and indirect effects. The direct effect is mediated by specific receptors found in cells of the osteoblast and osteoclast lineages. The effects of estrogen on osteoclasts are in part direct and in part mediated through osteoblasts. Some indirect effects of estrogen result from its enhancing the expression of growth factors like insulin like growth factor (IGF1) and transforming growth factor- (TGF-), and of cytokines, others from its inhibition of prostaglandin production by bone cells. Thus, the major effect of estrogen may be to inhibit bone resorption, but it may also have the additional effect of stimulating bone formation.

Host and bacterial factors involved in bone resorption:

The substance that can induce bone resorption in periodontal disease come from 2 sources:

Bacterial Factors:
Capsular and surface associated material, Lipopolysaccharides, Lipoteichoic acids, Peptidoglycans, Muramyll dipeptide, Lipoprotein. Substances from bacteria include Lipopolysaccharides (LPS) from gram negative bacteria, lipoteichoic acid from Actinomyces viscosus, peptidoglycan, Muramyll dipeptide (MDP), bacterial lipoprotein and capsular or surface associated

material (SAM) from gram- negative bacteria have the potency to cause resorption in vitro. It also varies with each source. LPS is 10 times more potent than lipoteichoic acid and capsular material is 1000 times more potent than the 3 materials above. There are also differences in effect from different bacterial sources of these materials. In this regard, LPS from Porphyromonas gingivalis is more active than, those from Actinobacllus actinomycetemcomitans, Capnocytophaga orchracea or Fusobacterium nucleatum. Capsular material or surface associated material (SAM) stimulates the production of PGE2 and collagenase from bone cells. The surface associated material from Prophyromonas gingivalis and Eikenella corrodens appear to achieve this by first releasing IL-1, which then stimulates the production of PGE2 and collagenase. The SAM from A actinomycetemcomitans, however, appears to mimic the action of IL-1 in its action. The main cytokine released from connective tissue and bone cells by these materials is IL-6 and it seems that this release is itself stimulated by IL-1. This is of particular relevance because IL-6 has been shown to stimulate the formation of osteoclasts. Some bacterial LPS, such -as that from Eikenella corrodens, also release these cytokines from these cells but most do not. LPS is however known to activate the complement cascade by the alternative pathway that generates prostaglandin.

Host Factors:
Inflammatory mediators, Prostaglandins e.g. PGE2, Leukotrienes, Bradykinin, Cytokines, Interleukin-1, Interleukin 6, Tumor Necrosis Factor. In recent years, it has become increasingly clear that many of the cellular events involved in bone resorption are modulated by a group of local factors (osteotropic cytokines), which have extremely potent effects on bone cells in both in vitro and in vivo systems. Many of the effects of local factors on bone resorption appear to be overlapping and are seemingly redundant; for example, lnterleukin-1 (IL-1), tumor necrosis factor-alpha (TNF-a), and lymphotoxin appear to affect bone resorption similarly. As we learn more about the mechanism of bone resorption, the role of each factor in the process will become clearer. Cytokine regulation is likely to be more important for trabecular bone than for

cortical bone because trabecular bone is closer to the marrow, which is a rich source of cytokines. Many of the potent osteotropic cytokines, such as IL-1, IL-6, tumour necrosis factor-a (TNF-a), and transforming growth factor-p (TGF-p), mediate a multiplicity of effects on bone cells. However, there are other factors, such as BMP, that have relatively specific effects on bone cells. Most of the osteotropic cytokines, such as IL-1, TNF, lymphotein, and IL-6, are clearly products of immune cells that are present in regions where bone modeling is actively occurring. However, stromal cells, as well as bone cells, also produce these factors. Bacteria, lipopolysaccharide, other cytokines and different hormones (estrogen and steroids) regulate the production of cytokines by osteoblasts. It has also been observed that cytokines and hormones can have synergistic effects on bone resorption. For example, the effect of IL-1 together with PTH on bone resorption is greater than the additive effects of either IL-1 or PTH alone. The hypothesis that local factors play a major role in regulating bone remodeling has been strengthened by recent data that directly implicate at least one of these cytokines in normal osteoclastic bone resorption. In mice with the op/op variant of osteopetrosis, there is a defect in the region coding for colony-stimulating factor (CSF) of the macrophage series (CSF-M), resulting in decreased CSF-M production. In this variant, the mice do not form functional osteoclasts. As a result, they do not form marrow cavities properly, and they develop osteopetrosis. If the mice are treated with CSF-M, the disease is reversed. Cytokines appear to play a major role in bone pathology. Solid tumors and carcinomas have been shown to produce IL-1. Cytokines have also been associated with the bone destruction seen in chronic inflammatory conditions, such as rheumatoid arthritis and periodontal disease. The observed increase in cytokines during these diseases has been suggested as the cause of increased localized osteolytic bone destruction.

lnterleukin-1 (IL-1): IL-1 is a powerful and potent bone-resorbing cytokine. It has

been found that IL-1 and IL-1 are equally potent in stimulating bone resorption and probably exert their effects on bone-resorbing cells in several ways.

They stimulate proliferation of precursor cells, but also probably act indirectly on mature cells to stimulate bone resorption. The effects of IL-1 probably occur by two mechanisms. One mechanism is the stimulation of the production and release of PGE2, there by stimulating bone. The second mechanism involves direct action of IL-1 on osteoclasts independent of PGE2 synthesis by 80 kda receptor.

lnterleukin-6 (IL-6):
In some experimental models, IL-6 appears to have no effects on bone resorption. However, in others, it stimulates bone resorption. IL-6 is also responsible for the formation of cells with an osteoclastic phenotype. Bone cells also have the ability to produce IL-6, which seems to be greater when the stimulus is by another cytokine,

Tumor necrosis factor (TNF) and Lymphotoxin:

Lymphotoxin and TNF are two closely related cytokines that have equivalent effects on bone cells. They are both multi-functional cytokines produced by activated Lymphocytes, and they share the same receptor. Their major effect on bone is to stimulate osteoclastic bone resorption. It has been suggested that part of the effect of TNF is mediated by PGE2, as well as by IL-6. TNF also affects cells with osteoblast; phenotypes and inhibits differentiated function and stimulates cell; proliferation. Production of TNF in some tumors, like squamous cell carcinomas, may be responsible for paraneoplastic syndromes.

Gamma interferon (IFN-):

Gamma interferon is a multi-functional cytokine, which in most biological; system has effects similar to TNF or IL-1. However, it has an effect on bone resorption that is opposite that of IL-1 and TNF. Gamma interferon is more effective in inhibiting IL-1 or TNF- a induced bone resorption than systemic hormones like PTH or 1,25(OH)2 D3. Further, it has been found in long-term marrow cell cultures that gamma interferon inhibits the formation of cells with the osteoclast phenotype.

Colony stimulating factors (CSF3):

CSF has ability to stimulate differentiation of osteoclast precursors info mature osteoclasts. Recently, it was found that there are a number of human and animal tumors associated with granulocytosis in which increased production of CSF3 is involved. In many of these tumors, hypercalcemia is associated with increased bone resorption. It is possible that CSF3 mediate their effects on osteoclast formation indirectly. For example, early studies showed that CSF stimulates IL-I production, which stimulates prostaglandin synthesis.

Prostaglandin and other arachidonic-acid metabolites:

A number of arachidonic-acid metabolites act as modulators of bone-cell function. These factors are produced by immune, marrow, and bone cells. Prostaglandins of the E series (PGE) are some of the first-described and best-tested stimulators of osteoclastic bone resorption. PGEs are slow acting, but powerful mediators of bone resorption and affect both active mature osteoclasts, as well as differentiated osteoclast precursors. The effect of PGE is local and has been shown to mediate the effects of other factors like epidermal growth factor (EGF) and transforming growth factor- (TGF-). PGE is produced by osteoblasts and has effects not just on bone resorption, but on bone formation as well. In vitro, it has been found that high doses of PGE are inhibitory, while low doses stimulate bone formation. However, in vvo it appears that the effect of PGE is clearly associated with an increase in periosteal bone formation, Arachidonic acid can be metabolized by an alternative enzyme system, 5-lipoxygenase, which also produces metabofites capable of stimulating bone resorption.

Other Products of Inflammation:

Heparin from mast cells can enhance bone resorption in tissue culture system induced by LPS and lipoteichoic acid, but cannot induce bone resorption on its own. Thrombin, an inflammatory mediator and end product of the blood coagulation cascade

is a potent bone-resorbing agent. Another inflammatory agent, bradykinin, evokes similar effects and it is independent of prostaglandin production.

ETIOLOGY OF BONE LOSS:

INFLAMMATION: The extension of inflammation to the supporting structures of a tooth may be modified by the pathogenic potential of plaque or by the resistance of the host. The latter includes immunologic activity and other tissue-related mechanisms, such as the degree of fibrosis of the gingiva, probably the width of the attached gingiva, and the reactive fibrogenesis and osteogenesis that occur peripheral to the inflammatory lesion. A fibrin- fibrinolytic system has been mentioned as "walling off' the advancing lesion. The pathway of the spread of inflammation is critical because it affects the pattern of bone destruction in periodontal disease.

Pathway of Inflammation:
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. Although the inflammatory infiltrate is concentrated in the marginal periodontium, the reaction is a much more diffuse one, often reaching the bone and eliciting a response before there is evidence of crestal resorption or loss of attachment. In the upper molar region, inflammation can extend to the maxillary sinus, resulting in thickening of the sinus mucosa. Interproximally, inflammation spreads in the loose connective tissue around the blood vessels, through the transseptal fibers, and then into the bone through vessel channels those perforate the crest of the interdental septum. The site at which the inflammation enters the bone depends on the location of the vessel channels. It may enter the interdental septum at the center of the crest, toward the side of the crest, or at the angle of the septum, and it may enter the bone through more than one channel. After reaching the marrow spaces, the inflammation may return from the bone into the periodontal ligament. Less frequently, the inflammation spreads from the gingival directly into the periodontal ligament and from there into the interdental septum.

Facially and lingually, inflammation from the gingiva spreads along the periosteal surface of the bone and penetrates into the marrow spaces through vessel channels in the outer cortex. Along its course from the gingiva to the bone, the inflammation destroys the gingiva and transseptal fibers, reducing them to disorganized granular fragments interspersed among the inflammatory cells and edema. However, there is a continuous tendency to recreate transseptal fibers across the crest of the interdental septum farther along the root as the bone destruction progresses. As a result, transseptal fibers are present, even in cases of extreme periodontal bone loss. The dense transseptal fibers are of clinical importance when surgical procedures are used to eradicate periodontal pockets. They form a firm covering over the bone, which is encountered after the superficial granulation tissue is removed. After inflammation reaches the bone by extension from the gingiva, it spreads into the marrow spaces and replaces the marrow with a leukocytic and fluid exudate, new blood vessels, and proliferating fibroblasts. Multinuclear osteoclasts and mononuclear phagocytes are increased in number, and the bone surfaces are lined with cove-like resorption lacunae. In the marrow spaces, resorption proceeds from within, causing first a thinning of the surrounding bony trabeculae and enlargement of the marrow spaces, followed by destruction of the bone and a reduction in bone height. Normally fatty bone marrow is partially or totally replaced by a fibrous type of marrow in the vicinity of the resorption. Bone destruction in periodontal disease is not a process of bone necrosis. It involves the activity of living cells along viable bone. When tissue necrosis and pus are present in periodontal disease, they occur in the soft tissue wall of periodontal pockets, not along the resorbing margin of the underlying bone. The amount of inflammatory infiltrate correlates with the degree of bone loss but not with the number of osteoclasts. However, the distance from the apical border of the inflammatory infiltrate to the alveolar bone crest correlates with both the number of osteoclasts on the alveolar crest and the total number of osteoclasts. But Irving, (1970) found that bone loss was not accompanied by osteoclasts and seemed to be more a result of gradual cessation of bone formation than of active resorption.

Locally produced bone resorption factors may have to be present in the proximity of the bone surface to be able to exert their action. Page and Schroeder (1982), on the basis of Waerhaug's (1980) measurements made on human autopsy specimens, postulated that there is a range of effectiveness of about 1.5 to 2.5 mm within which bacteria/ plaque can induce loss of bone. Beyond 2.5 mm there is no effect; interproximal angular defects can appear only in spaces wider than 2.5 mm because narrower spaces would be destroyed entirely. Tal (1984) corroborated this with measurements in human patients. Large defects far exceeding 2.5 mm from the tooth surface may be caused by the presence of bacteria in the tissues.

Mechanisms of Bone Destruction:

Many investigations have been conducted and many explanations considered, but the mechanisms by which inflammation and/or plaque-derived products destroy bone in inflammatory periodontal, disease have not yet been determined. There are several possible pathways by which products in plaque absorbed by periodontal tissues could cause alveolar bone loss (Hausman, 1974). 1. Absorbable products from plaque could stimulate bone progenitor cells in the periodontium to differentiate into osteoclasts, which resorb alveolar bone. 2. Absorbable products from plaque as, for example, complexing agents and hydrolytic enzymes could destroy alveolar bone through non-cellular mechanism by dissolving bone mineral and hydrolyzing the organic matrix. 3. a) Absorbable products from plaque could stimulate cells within the gingival to release mediators, which in turn could trigger bone progenitor cells to differentiate into bone resorbing osteoclasts. b) Gingival cells in response to plaque products could release agents which by themselves have no effect on bone, but could potentiate as co-factors other bone resorptive agents. c) Gingival cells could release agents, which destroy bone by direct chemical action without osteoclasts.

Periods of Destruction:
Periodontal destruction occurs in an episodic, intermittent fashion, with periods of inactivity or quiescence. The destructive periods result in loss of collagen and alveolar bone with deepening of the periodontal pocket. The reasons for the onset of destructive periods have not been totally elucidated, although the following theories have been offered: 1. Bursts of destructive activity are associated with subgingival ulceration and an acute inflammatory reaction, resulting in rapid loss of alveolar bone. 2. Bursts of destructive activity coincide with the conversion of a predominately T- lymphocyte lesion to one with predominance of B lymphocyte-plasma cell infiltrate. 3. Periods of exacerbation are associated with an increase of the loose, unattached, motile, gram-negative, anaerobic pocket flora, and periods of remission coincide with the formation of a dense, unattached, non-motile, gram-positive flora with a tendency to mineralize. 4. Tissue invasion by one or several bacterial species is followed by an advanced local host defense that controls the attack.

BONE LOSS IN PERIODONTITIS:

Periodontitis is the most common type of periodontal disease. It results from extension of the inflammatory process initiated in the gingiva to the supporting structures of the tooth. CHRONIC PERIODONTITIS: C/F: The characteristic findings in slowly progressive periodontitis are gingival inflammation, which results from the accumulation of plaque, and loss of periodontal attachment and alveolar bone, which results in formation of a pocket. Pocket depths are variable, and both horizontal and angular bone loss can be found. Tooth mobility often appears in advanced cases when bone loss has been considerable. Therefore, can be diagnosed clinically by the detection of chronic inflammatory changes in the marginal gingiva and the presence of periodontal pockets; it is diagnosed radiographically by evidence of bone loss.

When trauma from occlusion coexists, a higher incidence of infrabony pockets, angular bone loss, widening of the periodontal ligament, and earlier and more severe tooth mobility are found. TYPES: Mild periodontitis is usually characterized by probing attachment loss of 2 to 4 mm, minimal furcation invasions, and little tooth mobility. Radiographic evidence of bone loss is minimal (usually less than 20% of the total attachment). This stage of involvement can be localized to several teeth or generalized to many areas throughout the mouth. Patients with moderate periodontitis exhibit 4 to 7 mm of probing attachment loss, early to moderate furcation invasions, and slight to moderate tooth mobility. Radiographically evident bone loss is usually horizontal and may consist of upto 40% of the total possible periodontal attachment on the tooth. Patients with severe periodontitis have a probing attachment loss of 7 mm or more with significant furcation invasions, often through and through. Radiographic bone loss exceeds 40%, and angular bony defects are seen. Purulent exudate can be present, along with bleeding on probing. AGGRESSIVE PERIODONTITS: C/F Clinically, there is a small amount of plaque, which forms a thin film on the tooth and rarely mineralizes to become calculus. The most common initial symptoms are mobility of the first molars and distolabial migration of the incisors. Bone loss is about 3-4 times faster than in chronic periodontitis. The progression of bone loss and attachment loss may be self-arresting. RADIOGRAPHIC FINDINGS: Vertical loss of alveolar bone around the first molars and incisors in otherwise healthy teenagers is a diagnostic sign of classic juvenile periodontitis. Radiographic findings include an "arc-shaped" loss of alveolar bone extending from the distal surface of the second premolar to the mesial surface of the second molar. There is evidence that the bone loss, is not the result of any development or congenital absence or defect.

Alveolar bone in patients in this age group develops normally with tooth eruption, and only subsequently does it undergo resorptive changes.

Generalized: C/F
Clinically characterized by generalized interproximal attachment loss effecting atleast three permanent teeth other than first molars and incisors. Two types of gingival tissue responses can be found. One is severe, acutely inflamed tissue, often proliferating, ulcerated, and fiery red. Bleeding may occur spontaneously or with slight stimulation. Suppuration may be an important feature. In other cases, the gingival tissues may appear pink, free of inflammation, stipplings may or may not be present. This tissue response coincides with the periods of quiescence in which bone level remains stationary. The age at onset of this disease ranges from the middle to late teens and to 30 years old. By 30 to 35 years of age, patients will have progressed to advanced bone loss. RADIOGRAPHIC FINDINGS The radiographic picture can range from severe bone loss associated with minimal number of teeth, to advanced bone loss affecting the majority of teeth NECROTIZING ULCERATIVE PERIODONTITIS: Non-aids type necrotizing ulcerative periodontitis: C/F NUP is characterized by deep interdental osseous craters, but deep "conventional" pockets are not found, because the ulcerative and necrotizing character of the gingival lesion destroys the junctional epithelium, removing the mechanism of pocket deepening. Lesions of NUP can lead to advanced bone loss, tooth mobility, and tooth loss. Aids-Associated Necrotizing Ulcerative Periodontitis: C/F Gingival and periodontal lesions are frequently found in patients with AIDS. These gingival and periodontal lesions in human immuno-deficiency virus positive patients appear to be similar to those seen in NUP in HIV-negative patients but frequently result in complications that are extremely rare in non-AIDS patients. These complications consist of large areas of soft tissue necrosis with exposure of bone and

sequestration of bone fragments, sometimes extending to the vestibular area and/or the palate and becoming necrotizing stomatitis. PROGRESSION Bone loss associated with HIV-positive NUP may be extremely rapid. Winkler and colleagues (1988) mention cases in which 10 mm of bone were lost in 3 months. REFRACTORY PERIODONTITIS: Cases that, for unknown reasons, do not respond to therapy and / or recur soon after adequate treatment have been referred to as refractory periodontitis. Deterioration in cases of refractory periodontitis occurs either by new involvement of additional teeth or by increased bone and attachment loss in previously treated areas. PERIODONTITIS AS A MANIFESTATION OF SYSTEMIC DISEASES: Severe periodontitis has been observed in individuals with various neutrophil disorders including Papillon-Lefevre syndrome, Down syndrome, neutropenias, Chediak- Higashi syndrome, hypophosphatasia, acute and subacute leukemia, and leukocyte adhesion deficiency. TRAUMA FROM OCCLUSION: Trauma from occlusion 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 and tension of the periodontal ligament and increased osteoclasts of alveolar bone to necrosis of the periodontal ligament and bone and resorption of bone and tooth structure. Trauma from occlusion results in funnelshaped widening of the crestal portion of the periodontal ligament.

FOOD IMPACTION:
Inter dental defects often occur where proximal are abnormal or absent. Pressure and irritation from food impaction contributes to inverse articture. In some instances the poor proximal relation ship may be the result of shift in bone position because of

extensive bone destruction preceding food impaction. In such cases food impaction is the complicating factor rather than the cause of bone destruction.s

SMOKING:
Various studies recently have advocated and proven the adverse effect of smoking on periodontium and subsequently on bone. Mechanism of Action: 1. Vasoconstriction: Nicotine may cause a vasoconstriction in the peripheral blood vessels, evidence of which comes from various sources including Bergstrom, (1991). 2. Effect on immune response: Smoking may have an adverse action on fibroblast function (Raulin etal. 1988). Chemotaxis and phagocytosis (Kraal et al. 1977) and immunogfobulin production (Johnson 1990). Nicotine increases intercellular adhesion molecule-l (ICAM-1) and endothelial leukocyte adhesion molecule-l (ELAM-I). These molecules may impede the recruitment of important host defense cells to the area of inflammation and microbial challenge. 3. Cytokines: Tappia et al. (1995) have shown that smokers had more TNF & and IL-6 following lipopolysaccharide stimulation. Bostrom et al. (1998) have reported that smokers had significantly higher TNF & levels in GCF than did non-smokers in untreated and treated periodontitis. Payne and Johnson et al. (1996), examined effects of nicotine alone and in combination with lipopolysaccharide on bone resorbing factors PGE and IL1- . They found up regulation of LPS-mediated monocyte secretion of PGE2 by nicotine cytokine overproduction may be a detrimental host response which predisposes an individual to periodontitis. 4. Humoral immune response: Antigens are presented by macrophages in context of class II major histocompatibility complex (MHC-II) surface molecules. It has been shown that alveolar macrophages from smokers exhibit reduced expression of MHC-II (Mancini et al, 1993). Smoking has been shown to reduce the concentration of serum IgG (Roberston et al.1984).

STRESS
There are many forms of stress, such as trauma, drug intoxication, and muscular

fatigue that may compromise the health of an individual. The systemic reactions that affect the body generally or produce an interrelated nonspecific tissue change resulting from continued exposure to stress have been termed the general adaptation syndrome. Selye (1936) considered GAS to be the basis for the pathogenesis of numerous diseases. syndrome is thought to be a group of psychological mechanisms that represent an attempt by the body to resist the damaging effects of stress. Three stages of the syndrome have been identified: 1. The initial response 2. The Adaptation to stress 3. The final stage marked by inability to maintain adaptation to stress. The inferior lobe of the pituitary gland and the adrenal cortex are extremely active during periods of' stress. They produce the morphologic functional changes that compromise the GAS. The adrenal glands are enlarged, with increased secretion of adrenocorticoid hormones; involution of lymphatic organs; hyalinization and inflammatory changes in blood vessels; gastrointestinal ulceration; and malignant nephrosclerosis. Thus the adaptive mechanisms of the body in response to stress may produce disease. Osteo-porosis of alveolar bone, epithelial sloughing, degeneration of the periodontal ligament, reduced osteoblastic activity, and the formation of periodontal pockets, as well as delayed wound healing of connective tissue and bone, have all been associated with stress. Acute necrotizing ulcerative gingivitis is the periodontai disease having a significant relationship to stress.

BONE FACTOR CONCEPT: The focal and systemic factors regulate the
physiologic equilibrium of bone. When there is general tendency toward bone resorption, bone loss initiated by local inflammatory processes may be magnified. This systemic influence on the response of alveolar bone has been termed the bone factor in periodontal disease. The bone factor concept, developed by Irving Glickman (1951), envisioned a systemic component in all cases of periodontal disease. In addition to the

amount and virulence 'of plaque bacteria, the nature of the systemic component, not its presence or absence, influences the severity of periodontal destruction. Although, the term bone factor is not in current use, the concept of a role played by systemic defense mechanisms has been validated, by various studies.

Classification of Bony Defects:

Pritchard (1965) classification:

Interproximal craters. In constint margins. Hemisepta. Furcation involvement. Intra bony defect (with three osseous wals). Combination of above. Fenestration. Dehiscence.

Glickman (1964):
Osseous craters. Intra bony defect. Bulbous bony contours. Hemisepta. In consistent margins. Ledges.

BONE DESTRUCTION PATTERNS IN PERIODONTAL DISEASE:

Nomenclature of deformities of the alveolar process: The proposed system of nomenclature for bony deformities caused by non-uniform loss of bone is based on the following basic terms: OSSEOUS CRATERS: Osseous craters are concavities in the crest of the interdental bone confined within the facial and lingual walls. Craters have been found to be make up about one third of all defects and about two thirds of all mandibular defects. They are twice as common in posterior segments as in anterior segments. The following reasons for the high frequency of interdental craters have been suggested. 1) The interdental area collects plaque and is difficult to clean. 2) The normal flat or even concave faciolingual shape of the interdental septum in lower molars may favor crater formation.

3) Vascular patterns from the gingiva to the center of the crest may provide a pathway for inflammation. TRENCH: This term is applied when such bone loss affects two or more three confluent surfaces of the same tooth. MOLT: When the previously described deformity involves all four surfaces of tooth it is described as a moat. RAMP: In its purest form the term ramp describes deformity that results when both alveolar bone and its supporting bone are lost to the same degree in such a manner that the margins of the deformity are at different levels. PLANE: This term is applied when both alveolar bone and supporting bone is lost to the same degree such that the margins of the deformity are at the same level. It can be considered horizontal bone loss about one tooth or portion of a tooth. HEMISEPTA: Sometimes the pattern of interproximal bone destruction is uneven and, instead of a crater, the mesial or distal half of an inter-alveolar septum remains. If marginal bone is thick and the cortical plates remain intact on the buccal and lingual surface, the defect is intrabony because the denuded tooth root is surrounded by bony walls. A hemiseptum often is associated with an inconsistent osseous margin. The marginal bone level may be unchanged on one surface and notched by resorption on the other, or both the vestibular and lingual surfaces may exhibit marginal bone loss. Hemisepta occur between anterior as well as posterior teeth, and they are found in combination with all other types of bony deformities. An intrabony deformity may be associated with a hemiseptum is the most difficult osseous defect to remove because bone must be excised from the mesial or distal surface of a root in the interproximal space where access and visibility are poor.

REVERSED ARCHITECTURE: These defects are produced by loss of interdental bone, including the facial and/or lingual plates, without concomitant loss of radicular bone, thereby reversing the normal maxilla. LEDGES: Ledges are plateau-like bone margins caused by resorption of thickened bony plates. 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 in the mandible. FENESTRATIONS AND DEHISCENCE: Isolated areas in which the root is denuded of bone and the root surface is covered only by periosteum and overlying gingiva are termed fenestrations. In these instances the marginal bone is intact. When the denuded areas extend through the marginal bone, the defect is called as dehiscence. Such defects occur approximately 20% of the teeth; they occur more often on the facial bone than on the lingual, are more common on anterior teeth than on posterior teeth, and are frequently bilateral. There is micro cause of these defects is not clear. Prominent root contours, malposition, and labial protrusion of the root combined with a thin bony plate are predisposing factors. Fenestration and dehiscence are important, because they may complicate the outcome of periodontal surgery. FURCATION INVOLVEMENT: The term furcation involvement refers to the invasion of the bifurcation and trifurcation of multirooted teeth by periodontal disease. The mandibular first molars are the nmost common sites, and the maxillary involvements increase with age. The denuded furcation may be visible clinically or covered by the walls of the pocket. The extent of involvement is determined by exploration with a blunt probe, along with a simultaneous blast of warm air to facilitate visualization. architecture. Such defects are more common in the

Furcation involvement has been classified as grade I II III and IV according to the amount of tissue destruction. Grade I is incipient bone loss Grade II is partial bone loss (cul-de-sac) Grade III is total bone with through-and-through opening of the furcation. Grade IV is similar to grade III, but with gingival recession exposing the furcation to view. The destructive pattern in a furcation involvement varies in different cases and with the degree of involvement. Bone loss around each individual root may be horizontal or angular, and very frequently a crater develops in the interradicular area.

MARGINAL DEFECTS:
THICKENED MARGIN: An enlargement of facial or lingual marginal alveolar plate, instead of a thin, tapering, pr slightly rounded bony margin. Irregular bone margin. Where there are abrupt irregularities in the scalloped level of marginal bone and interdental septa. MARGINAL GUTTER: A shallow linear defect between marginal bone of the radical cortical plate or interdental crest, extending the length of one or more root surfaces, usually formed by resorption of the socket side of the plate and deposition on the facial surface. HORIZONTAL BONE LOSS: This is the most common pattern of bone loss in periodontal disease the bone is reduced in height, but the bone margin remains roughly perpendicular to the tooth surface. The interdental septa and facial and lingual plates are affected, but not necessarily to an equal degree around the same tooth. VERTICAL BONE LOSS OR ANGULAR DEFECTS: Vertical or angular defects are those that occur in an oblique direction, leaving a hollowed-out through in the bone along side the root; the base of the defect is located apical to the surrounding bone. In

many instances angular defects have accompanying infra bony pocket: such pocket always has an underlying angular defect. Angular defects are classified as: 1) Three wall bony defect bordered by one tooth surface and three osseous surfaces. 2) Two walled bony defect (inter dental creater) bordered by two tooth surface and two osseous surfaces. (One facial and one lingual). 3) One walled bony defect bordered by two tooth surface and one osseous surfaces (facial or lingual) and soft tissue. d. Combinations

DIAGNOSIS
Clinical: Periodontal probing and exploration are key expects of clinical examination. Careful probing reveals the presence of pocket depth greater than that of a normal gingival sulcus, the location of the base of the pocket relative to the mucogingival Junction and attachment level on adjacent teeth, the number of bony walls and the presence of furcation defects.Transgingival probing, or sounding, under focal anesthesia confirms the extent and configuration of the intrabony component of the pocket or of furcation defects. The probe should be "walked" along the tissue-tooth interface, so as to feel the bony topography. The probe may also be passed horizontally through the tissue to provide three-dimensional information regarding bony contours. RADIOGRAPHIC DIAGNOSIS Dental radiographs are the traditional method used to assess the destruction of alveolar bone associated with periodontitis. Although radiographs cannot accurately reflect the bony morphology buccal and lingual, they provide useful information on interproximal bone levels. However, even at this level, the exact topography of defects cannot be assessed accurately from radiographs. It is well known that substantial volumes of alveolar bone must be destroyed before the loss is detectable in radiographs; more than 30% of the bone mass at the alveolarcrestmust is lost for a change in bone height to be recognized on radiographs. Therefore, radiographs will seldom reveal bone loss when sufficient loss has not taken

place. Thus, radiographs are not sensitive. Radiographic and nuclear medicine techniques have been developed to obtain a higher degree of sensitivity to minor bone changes. Various methods radiographic diagnosis include photodensitometric analysis digital radiography, subtraction radiography, CADIA, I125Absorptionmetry, nuclear medicine.

Conclusion:
Prevention is better than cure so there is a need for early diagnosis and identification of these factors such as local factors, TFO, Smoking, Stress, Systemic Disorders etc prevention of which would further prevent progression of the disease.

REFERENCE: 1) Carranzas Clinical Periodontology 9th Edition. 2) Perio 2000, 2000, 22, 8-21. 3) Perio 2000, 2002, 30, 91-103.

4) Periodontal Disease 2nd Edition Schluger. 5) JP 1974, 45, 88-92. 6) JP 1983, 55, 336-340. 7) Perio 2000, 1997, 14, 158.

COLLEGE OF DENTAL SCIENCES DEPARTMENT OF PERIODONTICS DAVANAGERE.

SEMINAR ON BONE LOSS AND PATTERNS OF BONE DISTRUCTION.

PRESENTED BY M. SESHA REDDY.