ALVEOLAR BONE IN HEALTH AND DISEASE

1. INTRODUCTION

2. OBJECTIVE

3. BONE IN GENERAL

CLASSIFICATION OF BONES

STRUCTURE OF BONE

OSSIFICATION METHODS

GROWTH OF BONE

4. ALVEOLAR BONE

5. ANATOMY OF ALVEOLAR BONE

6. FUNCTIONS

7. EMBRYOGENESIS

8. STRUCTURAL HEIRARCHY

9. REMODELLING AND REPAIR

10. MECHANISM OF BONE RESORPTION

11. ALVEOLAR BONE IN DISEASE

12. CONCLUSION

INTRODUCTION:

Alveolar bone is a specialized part of the mandibular and maxillary bones that forms the primary support structure for teeth. Although fundamentally comparable to other bone tissues in the body, alveolar bone is subjected to continual and rapid remodeling associated with tooth eruption and subsequently the functional demands of mastication. The ability of alveolar bone to undergo rapid remodeling is also important for positional adaptation of the teeth but may be detrimental to the progression of periodontal disease. Much of the current information on alveolar bone must be extrapolated from studies of other bone tissues.

BONE IN GENERAL:

There are two types of bone tissue: compact and spongy. The names imply that the two types of differ in density, or how tightly the tissue is packed together.

Compact Bone

Compact bone consists of closely packed osteons or haversian systems. The osteon consists of a central canal called the osteonic (haversian) canal, which is surrounded by concentric rings (lamellae) of matrix. Between the rings of matrix, the bone cells (osteocytes) are located in spaces called lacunae. Small channels (canaliculi) radiate from the lacunae to the osteonic (haversian) canal to provide passageways through the hard matrix. In compact bone, the haversian systems are packed tightly together to form what appears to be a solid mass. The osteonic canals contain blood vessels that are parallel to the long axis of the bone. These blood vessels interconnect, by way of perforating canals, with vessels on the surface of the bone.

ALVEOLAR PROCESS

The alveolar process is the part of maxilla or mandible that forms and supports the teeth. As a result of functional adaptation, two parts of alveolar process may be distinguished.

1. The alveolar bone proper (socket wall)

The alveolar bone proper consists of thin lamella of bone (cortical bone) surrounding the root and bundle bone. Sharpey’s fibers of periodontal ligament are embedded in bundle bone. Some sharpey’s fibers are calcified completely, but most of them contain a central uncalcified core.

2. The supporting bone. The supporting bone surrounds the alveolar bone proper and provides

additional functional support. Supporting bone consists of (1) the compact cortical plates of vestibular and oral surfaces of alveolar processes (outer cortical plates) and (2) the cancellous, trabecular, or spongy bone sandwiched between these cortical plates and the alveolar bone proper (inner cortical plate).

In roentgenograms the alveolar bone proper appears as an opaque line called the lamina dura. The alveolar bone proper is perforated by many openings through which the blood vessels, lymphatics and nerves of periodontal ligament pass. It is also called the cribriform plate because of perforations. The inner cortical plate contains the sharpey’s fibers of periodontal ligament fibers.

The inner and outer cortical plates meet at alveolar crest where they may fuse. The inner cortical plates of adjacent alveoli are also fused interdentally. The alveolar crest more or less parallels the outline of the cervical margin of the enamel 1-3mm apical to it, with a greater distance seen in older individuals.

The interdental septa are the bony partitions that separate adjacent alveoli. Coronally, at the cervical region, the septa are thinner and here the inner cortical palates are fused and cancellous bone is frequently missing. Apically the septa are thicker and generally contain intervening cancellous bone and some times haversian bone.

The shape of the alveolar crest, under normal conditions, depends on the contour of enamel of adjacent teeth, the relative position of the adjacent CEJ, the degree of eruption of teeth, the vertical positioning of the teeth, and the oro-vestibular depth of the teeth. In general, the bone about each tooth follows the contour of the cervical line.

FUNCTION:

The alveolar bone proper adapts itself to the functional demands of the teeth in a dynamic manner. It is formed for the express purpose of supporting and attaching the teeth. The alveolar process depends on the presence of teeth for its existence. If teeth fail to develop, it will not form. If teeth are lost or extracted, it will tend to involute.

ANATOMY:

Roentgenograms

Roentgenograms of cross-sections of the alveolar process show its cortical and cancellous portions. The cortical plates are generally thicker in the mandible. The cortical plates and the cancellous bone are also generally thicker on the oral aspects of the mandible and the maxilla, but there is individual variation.

Anteriorly, along the vestibular aspect of the alveolar arch, is the depression of the incisive fossa, bordered distally by the cuspid eminences. Here the bone is thin, and there may be little or no cancellous bone. Posteriorly, in the premolar and molar regions, the bone is thicker, and generally, cancellous bone separates the cortical plate from the alveolar bone proper.

Thickness of alveolar process

Since the teeth are responsible for the alveolar process, it general form and shape follow the arrangement of the dentition. In addition the thickness of alveolar bone has a direct bearing with external contour. When the process is thin interdental depressions can be seen between roots and there are prominences over roots. Malposition of teeth also affects the thickness of alveolar process.

Alveolar crest:

The margin of alveolar process is normally rounded or beaded. Occasionally the margin ends in fine sharp edge. This occurs when the bone is extremely thin for example on the vestibular surface of incisors and canines.

The contour of crestal bone margin is generally scalloped. If root surface is flat then crest is also flat. If root surface has convex surface then crestal bone margin follows convexity giving scalloping appearance.

Form of interdental septum

The form of interdental septum follows the alignment of adjacent CEJs. The septa in anterior region form peaks. In posterior region they are wide and flat. When the teeth are in close approximation the interdental septa is absent. This is seen mostly between the distobuccal root of maxillary 1st molar and mesiobuccal root of adjacent second molar. The distance between crest of alveolar bone to CEJ in young adults varies between 0.75 – 1.49. This distance increases with age to an average 2.81.

Relationship with maxillary sinus:

The maxillary sinus is separated from the root apices of molars in maxilla by thin osseous partition. With the age sinus grows towards roots decreasing the thickness of this partition. After extraction of molar the sinus grows more rapidly. The cortical plate between teeth next to extraction socket and the sinus may become paper thin. This may lead to oroantral fistulas during surgical procedures involving such regions.

Dehiscence & Fenestrations

Dehiscence is dipping of crestal bone exposing the root surface. Fenestration is circumscribed hole in the cortical plate over the root and does not communicate with crestal margin. It varies in size and can be located any where along the root surface.

EMBRYOGENESIS OF ALVEOLAR BONE:

The alveolar bone of maxilla is formed by mesenchyme. The mandibular alveolar bone develops from the mesenchyme of first branchial arch initially adjacent to Meckel’s cartilage. The genesis of alveolar bone is similar to intramembranous ossification else where in the body.

Mesenchymal cells form aggregations that differentiate into osteoblasts. According to Newman this is in response to adhesion molecules (eg, fibronectin) and soluble signals. These two are members of transforming growth factor –beta (TGF-β) family. The regional proclivity for direct, intramembranous bone formation in mandibulocranial complex has not yet been explained satisfactorily. It is accepted that bone morphogenic proteins (BMPs), a subgroup within TGF-β family promote osteoblastic differentiation from mesenchymal cells. Perhaps there is a concentration gradient of BMPs that favors intra membranous bone formation in this area during 5th and 6th week of gestation. Ripamonti described that basic FGF on the surface of vascular endothelium, type IV collagen and matrix components of blood vessels bind to BMP-3, BMP-4 and BMP-7. Thus the BMPs concentration gradient is greater in the mandibulocranial complex. Where as in endochondral bone sites angiogenesis inhibitors (protamine) down regulates the bFGF synthesis. This diminishes vasularity in endochondral bone forming sites and cartilage is formed as described by Taylor and Folkman. Other factors that may inhibit vascularisation here are interferon-β, IL-12, angiostatin.

Osteoblasts secrete matrix vesicles. The process of calcifying extracellular matrix begins in the centre of spherule of aggregated osteoblasts, collagen, proteoglycans, and matrix vesicles. The first sign of hydroxyapatite calcification is seen within matrix vesicle. Later hydroxyapatite crystals growing by epitaxy form spheroids. These are bone nodules that coalesce into seams of woven bone and extend in, on and between collagen fibrils. As the first deciduous tooth buds appear in maxilla and mandible, Woven bone spicules loosely surround each developing tooth. Trabeculae of woven bone grow and anastomose. The osteoblasts are trapped in growing calcified matrix and are now termed osteocytes.

On the trabecular surfaces of woven bone, collagen is secreted in oriented sheets that calcify by epitaxy from the hydroxyapatite crystals in the woven bone. The successive layers of collagen, each sheet oriented in different plane, give the bone leaflet-on-leaflet appearance called lamellar bone. Shortly after the first woven bone has formed, osteoclasts are found on the surfaces of both the woven and lamellar bone of trabeculae. They begin the process of resorption and with osteoblasts, remodeling the bone into its proper shape at each stage of development.

STRUCTURAL HIERARCHY OF ALVEOLAR BONE:

Microstructure: alveolar bone may be categorized into four microstructural components: cells, inorganic matrix, organic matrix and soluble signaling factors.

Bone cells: bone cells include Osteoblasts, Osteocytes, and Osteoclasts.

1. OSTEOBLASTS:

Osteoblasts are derived from mesenchymal lineage. Actively secreting osteoblasts are lined up along the osseous surface as sheet of plump, basophilic cells with large nuclei. They have well developed Golgi regions with a dense network of rough –surfaced endoplasmic reticulum. Ctyoplasmic extensions may traverse the osteoid layer to make contact with those of adjacent osteocytes. Where active osteogenesis is absent, the bone surface may be lined with flattened cells lacking a rough endoplasmic reticulum. They are considered to be osteoprogenitor cells. They are capable of dividing into preosteoblasts, which no longer able to divide and may evolve further into osteoblasts.

The progression of stem cells to end stage osteoblasts may take two roots one leading to determined osteoprogenitor cells. The determined lineage is associated with cell condensation and may be responsible for bone formation during embryogenesis, whereas during fracture repair an inducible population may be susceptible to soluble inductive morphogens- polypeptides that promote expression of distinctive cell phenotypes. The effect being dose related.

When bone is injured as a consequence of surgical intervention and trauma, a population of local cells restores osseous form and function through recapitulation of embryonic events the local cells are determined osteoprogenitor, resident in the cambial layers of the periosteum, endosteum and dura, and inducible osteoprogenitor cells , such as pericytes that arrive at injury locus about 3-5 days after injury via transit in developing capillary sprouts. Pericytes also may convert to osteoblasts following interactions with endogenous BMPs.

Further more, according to Brighton and colleagues, a population of polymorphic mesenchymal cells may appear as early as 12 hours following

fracture, providing a preosteoblastic cell resource. Moreover mesenchymal stem cells within the bone marrow contribute to the complement of cells present within the repair blastema. These cells, which possess multilineage potential, can convert either to cartilage – forming chondrocytes or bone -forming osteoblasts depending on the presence of environmental cues such as nutrients supply, specific growth factors, blood vessels and mechanical stability. It already has been established that marrow-- derived inducible osteoprogenitor cells undergo osteoblastic differentiation in response to BMPs and other naturally occurring growth factors.

The osteoblasts secrete soluble signaling factors eg, BMPs, TGF-β, insulin like growth factor I and II, interleukin-1 and platelet derived growth factors and osteoid. For remodeling the osteoid produced is produced at the rate of 2-3µm/ day at a thickness of 20 µm. the osteiod mineralizes at the rate of 1-2µm/day.

2. OSTEOCYTES:

Osteocytes are derived from osteoblasts and are capable of resorbing and forming bone. Osteocytes have reduced cytoplasm and cellular organelles when compared to osteoblasts. Their Ctyoplasmic processes radiate from the cell body though numerous canaliculi to connect with cells in adjacent lacunae. Osteocytes respond to changing hormonal levels. They are able to resorb bone lacunar walls (osteocytic osteolysis) and to deposit new bone.

Osteocytes are relatively inactive cells, yet their subdued metabolic activity is crucial to bone viability and sustain homeostasis (maintenance of constant internal conditions within the body). All the three cells of bone play important role in calcium regulation, homeostasis, remodeling and repair. Their life span is for many years, perhaps even decades.

3. OSTEOCLASTS:

Osteoblasts are multinucleated cells in depressions of bone surface. They are the main cells capable of bone resorption. The surface facing bone is highly convoluted forming a “ruffled border.” The cytoplasm of osteoclasts contains numerous vesicles, lysosomes, and mitochondria, but little endoplasmic reticulum. The size and concentration of vesicles increase in proximity to the ruffled border, which is the zone where active bone resorption takes place. Free apatite crystallites and frayed collagen fibrils are found between the Ctyoplasmic extensions of these cells. The periphery of the ruffled border, by contrast, closely contacts the bone surface and seals the resorptive, ruffled border zone. This region is referred to as the clear zone because the adjacent cytoplasm lacks organelles and particulate elements. The cavities formed after resorptions are called Howship lacunae.

They originate from macrophages of hemopoietic origin. These cells fuse to form typical multinucleated cells or they may participate in bone resorption as single nuclear cells. Fibroblast derived collagenase also contribute to bone resorption.

The number of osteoblasts may be increased by parathyroid hormone and is decreased by calcitonin. 1, 25-Dihydroxycalciferol increases the resorptive activity without increasing cell number. In addition to these local factors such as osteoclasts- activating factor (OAF), lymphokines (IL-1, -3,-6, and -11) and prostaglandins also influence bone resorption

BONE MATRIX:

The matrix of bone is of two types i.e. organic and inorganic matrix.

Organic matrix:

The organic matrix constitutes 35% of dry weight of bone. It can be divided into collagenous and noncollagenous components. Collagenous part contains type I collagen (about 90%). They form fibrous backbone of extra cellular matrix (ECM). The rest 10% are noncollagenous proteins. They include proteoglycans, glycoproteins and BMPs.

The proteoglycans are composed of glycosaminoglycans (GAGs) covalently linked to core proteins. The GAGs contain repeating carbohydrate units that are sulfated; eg, chondroitin sulfate, dermatan sulfate, keratin sulfate, hyluronic acid and heparin sulfate. The examples of proteoglycans are fibromodulin, osteoadherin, osteoglycin. Examples of glycoproteins are fibronectin, osteonectin, osteopontin, fibrilin. These noncollagenous proteins may modulate cellular attachment.

The ability of bone to induce new cartilage and bone formation is from the action of the BMPs.

Inorganic matrix:

It constitutes for 60-70% of dry weight of bone i.e. 2/3 of matrix. The inorganic matter is composed principally of minerals calcium, phosphate along with hydroxyl, carbonates, citrate and trace amount of other ions, such as sodium, magnesium, and fluorine. They form hydroxyl apatite crystals Ca10 (PO4)6(OH) 2. These apatite crystals are arranged parallel to the long axes of collagen fibers and appear to be deposited on and within these fibers. In this fashion the bone can withstand the heavy mechanical stresses applied to it during function.

REMODELING AND REPAIR OF BONE:

In normal physiology, there is a coupling of resorption and formation in the bone remodeling sequence. In the various metabolic bone diseases, there are abnormalities in the coordinated activity of the osteoclastic and osteoblastic cells. Likewise, in a pathological state such as inflammation, there is an uncoupling of these activities resulting in a net loss of bone. A complex cascade of events involving a host of autocrine and paracrine factors is involved in the regulation of bone metabolism.

The structure of alveolar bone proper varies on different sides of tooth, with different functional demands. Under physiologic conditions teeth migrate continuously in mesial direction toward the midline. This is called physiologic mesial drift. The migration leads to resorption on mesial side and new bone formation on tension side i.e., distal side.

Some portions of bone surface may be covered by a thin layer old new bone that anchors short sharpey’s fibers. This new bone is formed during relatively brief periods of bone deposition, which allows the root to remain

anchored to bone despite a predominance of bone resorption over deposition. This new bone is separated from old bone by reversal line. Reversal lines tend to have scalloped outline that separates them last resorptive activity area. This outline is result of resorptive bays created by osteoclasts.

MECHANISM OF BONE RESORPTION

1. Hydrolytic enzyme mechanism 2. Acidic environment mechanism or proton pump mechanism

Ultrastructural evidence suggests that osteoclasts first solubilize the

mineral phase and next cause dissolution of the organic phase of the matrix. The resorption area is defined beneath the ruffled border as a highly specialized region of cytoplasmic infolding on the plasma membrane, outlined by a sealing zone or clear zone. The clear zone has been shown to contain podosomes, specialized protrusions of the ventral membrane of osteoclasts, which adhere to the calcified substrate to be broken down. It has been demonstrated that the clear zone contains a network of actin-containing microfilaments. It has been demonstrated that lowering of extracellular calcium promotes podosome formation, but raising intracellular calcium by blocking the calcium pumps induces podosome disappearance and formation of membrane ruffles. An electrogenic H + -transporting, ATPase-driven proton pump similar to renal tubular epithelial transport systems establishes a pH gradient. Intracellular pH regulation is most likely achieved by carbonic anhydrase which has been shown to be abundant in osteoclast cytoplasm. Bicarbonate, generated by this carbonic anhydrase, appears to be secreted from the basolateral membrane via HCO3/CL- exchange. The protons released into the functionally extracellular lysomal compartment may solubilize bone mineral and create a suitable pH for lysosomal enzyme activity on the demineralized organic bone matrix.

ALVEOLAR BONE IN DISEASE:

The alveolar bone destruction can be divided into following types:1. Bone destruction caused by extension of gingival inflammation.2. bone destruction caused by trauma from occlusion3. bone destruction caused by systemic disorders

Bone destruction caused by systemic disorders:

Osteopenia / osteoporosis: Osteopenia is characterized by a reduction in bone mass, whereas osteoporosis

is the most severe degree of osteopenia which leads to pain, deformity, or fracture. Osteoporosis is a physiological, gender, and age-related condition resulting from bone mineral content loss and structural change in bones. The rate of bone mineral loss is approximately two times greater in women than men. In women, post-menopausal osteoporosis is a heterogeneous disorder which begins after natural or surgical menopause

Alveolar Bone Loss Progression in Diabetes:

It suggested that poorer glycemic control leads to both an increased risk for alveolar bone loss and more severe progression over those without type 2 DM.

1. Polymorphonuclear Leukocyte Function.2. Collagen Metabolism and Advanced Glycation End products.

Vitamin D deficiency:Vitamin D or calciferol is essential for the absorption of calcium from the

gastrointestinal tract and the maintenance of the calcium phosphorous balance.Experimental studies in animals showed that in osteomalacia, there is rapid,

generalized severe osteoclastic resorption of alveolar bone, proliferation of fibroblasts that replace bone and marrow, and new bone formation around the remnants of unresorbed bony trabeculae. Radiologically there is generalized partial to complete loss of lamina dura and reduced density of supporting bone, loss of trabeculae. Increased radiolucence of trabecular interstices and increased prominence of remaining trabeculae.

Hyperparathyroidism:Oral changes include malocclusion and tooth mobility, radiographic evidence

of alveolar osteoporosis with closely meshed trabeculae, widening of the lamina dura, and radiolucent cyst like spaces. Bone cysts become filled with fibrous tissue with abundant hemosiderin- laden macrophages and giant cells. They have been called brown tumors, although they are not really tumors but reparative giant cell granulomas. This disease is called osteitis fibrosa cystica or Von Recklinghausen’s disease. Other diseases in which it may occur are Paget’s disease, fibrous dysplasia, and osteomalacia.

Sex hormones:Ovirectomy results in osteoporosis of alveolar bone, reduced cementum

formation, and reduced fiber density and cellularity of periodontal ligament in young adult mice, but not in older animals. The gingival epithelium is atrophic in estrogen- deficient animals.

Systemic administration of testesterone retards the down growth of sulcular epithelium over cementum, stimulates osteoblastic activity in alveolar bone; increases the cellularity of periodontal ligament; and restores osteoblastic activity, which is depressed by hypophysectomy

Hematological disorders:In leukemic mice , the presence of infiltrate in marrow spaces and the

periodontal ligament results in osteoporosis of alveolar bone with destruction of the supporting bone and disappearance of periodontal fibers.

In Sickle cell anemia generalized osteoporosis of the jaws, with a peculiar stepladder alignment of the trabeculae of interdental septa and pallor and yellowish discoloration of oral mucosa. On the other way periodontal infections may precipitate sickle cell crisis.

Conclusion:

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

References:

1. Clinical Periodontology by Carranza, Newman and Takei.2. Periodontics by Grant, Stern and Listgarten.

Alveolar Bone

Seminar byDr. N.Upendra Natha Reddy

Postgraduate Student

2004-2007