Alveolar bone of Human with its clinical considerations

Aloveolar bone, ossification, age changes, clinical considerations

1. Alveolar bone SUBMITTED BY: Dr.Enna Dept.of Pediatric and Preventive Dentistry 1

2. CON T EN T S  Introduction  Classification  Composition  Structure of bone  Histology  Bone formation  Bone resorption  Bone remodelling  Clinical application  Vascular supply  Lymphatic drainage  Nerve supply  Bone marrow  Alveolar bone diseases 2

3. INTROD U CTION  Bone is a specialized, rigid, mineralized connective tissue .  Highly vascular.  Forms the body skeleton.  It is the hardest structure of the body. 3

4. FUNCTIONS  It forms framework and shape to the body .  Protects the soft tissue and vital organs .  Gives attachment to muscles and tendons .  Provides leverage for movement .  Acts as a reservoir for metabolic calcium and phosphate .  Acts as a site of production and storage of red blood cells .  Provides resilience and resists stress to the body. 4

5. CLASSIFIC A TION BASED ON M I C R O S C O PIC STRUCT U RE BASED ON DE V E L O PM E NT IMMATURE M A TU R E BASED ON SHAPE LONG SHO R T FL A T IRREGULAR S E S A M OID ENDOCHONDRAL INTRA-MEMBRANOUS 5

6. BASED ON MICROSCOPIC STRUCTURE  MATURE BONE: I. COMPACT BONE (CORTICAL/LAMELLAR)  Tightly packed osteons or haversian systems;  Arranged in layers;  Combination of cortex and medullary canal of long bones provides strength and low weight. 6

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8. II.CANCELLOUS BONE (SPONGY/TRABECULAR)  Honeycomb appearance ;  Large marrow cavities;  Bony elements or trabeculae arranged in form of bars or plates;  Provides additional strength to cortices;  Supports bone marrow. 8

9. IMMATURE BONE  WOVEN BONE :  First formed bone;  Irregularly oriented collagen fibers;  Forms rapidly;  Seen in alveolar bone and during healing of fractures . 9

10. BASED ON SHAPE  Long bone  Longer than wider;  Shaft-diaphysis;  Ends-epiphysis;  Diaphysis -central cavity (yellow marrow);  Epiphysis- compact bone at the periphery, spongy bone at the centre. 10

11.  Epiphysial line (remnant of epiphysial line) is present between diaphysis and epiphysis in adult bone.  Very few trabeculae.  Examples: radius, ulna, femur, tibia . 11

12. Short bones :  Equal in length and width.  Cube shaped.  Consist of spongy bone covered by thin layer of compact bone Examples: carpels of wrist ,Tarsals of ankle. 12

13. Flat bones : Thin, flat, curved . No marrow cavity . Spongy bone present between upper and lower layer of compact bone . Example: sternum, scapula, roof of skull . 13

14. Irregular bones Complex shapes Notched or with ridges Spongy bone covered with thin layer of compact bone Example: mandible Sesamoid bone Develop in tendons where there is pressure, tension, friction. Example: patella 14

15. COMPOSITION 15

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18. ALVEOLAR BONE  It is defined as the part of the maxilla and the mandible that forms and supports the sockets of teeth.  Alveolar bone is subjected to continual and rapid remodeling associated with tooth eruption and subsequently the functional demands of mastication.  The size, shape , location and function of the teeth determine the morphology of the alveolar bone. 18

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20. Functions :  Houses the roots of teeth 20

21.  Anchors r oots of te e th to a l veoli with the help o f sha r pey ’ s fibers 21

22.  Supplies vessels to PDL; 22

23.  Organizes eruption of teeth; 23

24. STRUCTURE OF ALVEOLAR BONE Cortical bone An external plate Haversian bone and compacted bone lamellae Alveolar bone proper Inner socket wall Thin co m pact bone Rad i o g ra p hs: lamina dura Cancellous tr a becul a e In t er d en t al septum Encl o sed within a compact bone 24

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30.  The bone which covers the root surfaces is considerably thicker at the palatal than at the buccal aspect of the jaw.  The walls of the socket are lined by cortical bone and the area between the socket and between the compact jaw bone wall is occupied by cancellous bone 30

31. PERIOSTEUM INNER LAYER  Composed of Osteoblasts surrounded by Osteoprog eni tor cells, which have the potential to differentiate into osteoblasts.  Inner layer is osteogenic layer. OUTER LAYER  This layer is rich in blood vessels and nerves and composed of collagen fibers and fibroblasts.  Outer layer is the fibrous layer. 31

32. ENDOSTEUM : Layers of differentiated osteogenic connective tissue cover all the bone surfaces. The Tissue covering the outer surface of the bone is periosteum. The Tissue lining the internal bone cavities is called endosteum. 32

33. Sharpey's fibers are the terminal ends of fibers that insert into the cementum and into the periosteum of the alveolar bone. Sharpey's fibers intensifies the continuity between the periodontal ligament fiber and the alveolar bone. 33

34. INTERDE N T AL SEPTUM: The interdental septum consists of cancellous bone bordered by socket wall cribriform plates of approximating teeth and the facial and lingual cortical plates. If the interdental space is narrow, the septum may consists of only the cribriform plate. 34

35. HISTOLOGY OF BONE 35

36.  RESTING LINES This lines has more regular appearance which denotes period of rest during bone formation.  REVERSAL LINES/ CEMENTING LINES : This cement line contains little or no collagen, and is strongly basophilic, because it has a high content of glycoproteins and proteoglycans. This lines has irregular lines which indicates area of bone resorption . It marks the limit of bone erosion prior to the formation of osteon . 36

37. Like other connective tissues, bone tissue contains an abundant matrix surrounding the cells. The matrix is about 25% water, 25% protein fibres and 50% mineral salts. There are 4 types of cells in bone tissue :- OSTEOPROGENITOR cells are unspecialized cells derived from mesenchyme , the tissue from which all connective tissues are derived. They undergo mitosis and develop into osteoblasts. They are found in the periosteum, endosteum and in canals that contains blood vessels. 37

38.  OSTEOBLASTS are the cells that form bone, but they have lost the ability to divide by mitosis . They secrete collagen and other organic components needed to build bone tissue.  The differentiation of osteoprogenitor cells into osteoblast is accelerated by some hormones and some bone proteins called Skeletal growth factors. FUNCTIONS :  Role in formation of bone matrix,  Role in calcification ( through the alkaline phosphatase enzymes)  Synthesis of proteins . 38

39. OSTEOCYTES these cells are concerned with maintenance of bone.  Small flattened and rounded cells embedded in bone lacunae.  Derived from mature Osteoblast . FUNCTIONS  Help to maintain the bone as living tissue because of there metabolic activity.  Maintain the exchange of calcium between the bone and ECF . 39

40. OSTEOCLASTS : Concerned with bone resorption .  Giant phagocytic multinucleated cells found in the lacunae of bone matrix.  Derived from hemopoietic stem cells via monocytes.( CFU-M) FUNCTIONS  Responsible for bone resorption during bone remodelling.  Synthesis and release of lysosomal enzymes necessary for bone resorption in to bone resorbing compartment. 40

41. RE G UL A TION OF OST E OB L AST AC T IVITY 41

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43. F AC T ORS AF F EC T ING OSTE O CL A ST ACTIVITY 43

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45. BONE FORMATION  Formation of bone, which appears to be linked with bone resorption to maintain bone mass, involves the proliferation and differentiation of stromal stem cells along an osteogenic pathway that leads to the formation of osteoblasts .  Osteoblasts synthesize the collagenous precursors of bone matrix and also regulate its mineralization . 45

46.  The process by which bone forms is called OSSIFICATION.  The skeleton of a human embryo is composed of fibrous connective tissue membrane formed by embryonic connective tissue (mesenchyme) and hyaline cartilage that are loosely shaped like bones. They provide supporting structure for ossification .  Ossification begins around the 6 th or 7 th week of embryonic life and continues throughout adulthood. 46

47.  Bone formation follows one of 2 patterns; In t ra m e m branous oss ificat i o n - refers to the f or m at i on of bone directly on or within the fibrous connective tissue membranes. Endochondral ossification- refers to the formation of bone in hyaline cartilage Maxilla forms by intramembranous ossification. Mandible forms partly by intramembranous and partly by intra cartilaginous ossification. Greater part of body, ramus, condyloid and coronoid process are intramembranous in origin. Only the tip of condyloid and coronoid process are of endochondral origin. 47

48. INT R A M EM B R A NOUS OSSIFICATION  https://www.youtube.com/watch?v=-dODanIem2Y 48

49. ENDOCHONDRAL OSSIFICATION 49

50. BONE RESORPTION  Removal of the mineral and organic components of extracellular matrix of bone under the action of osteolytic cells especially osteoclasts .  Sequence of bone resorption:  1 st phase : Formation of osteoclast progenitors in hematopoietic tissues.  Their vascular dissemination.  Generation of resting preosteoclasts and osteoclast in bone. 50

51.  2 nd phase Activation of osteoclasts at the surface of bone.  3 rd phase Activated osteoclasts resorbing bone. 51

52. Alterations in osteoclasts  Osteoclasts create cavities called howships lacunae which are shallow troughs with an irregular shape. Osteoclasts undergo changes just before resorption : Development of ruffled border Many infoldings of cell membrane resulting in fingerlike projections of the cytoplasm creating an extensive surface suited for resorption. Sealing zone of the plasma membrane At the periphery of the ruffled border plasma membrane is smooth and closely apposed to bone surface. 52

53.  Cytoplasm contains contractile actin microfilaments surrounded by 2 vinculin rings .  This region is called sealing zone or clear zone .  Facilitates attachment of osteoclast to resorption sites.  Creates an isolated microenvironment for resorption.  Osteoclasts binds to bone by Integrin and Vitronectin. 53

54. Degradation of organic matrix  Digestion of organic component occurs by osteolytic enzymes like Cathepsin K and matrix metalloproteinase secreted by osteoclasts.  Cathepsin K degrades major amount of Type 1 collagen and non collagenous proteins.  MMP9 req u ired for o steoclast m igration, b o n e resorption and osteoclas t differentiation . 54

55. Removal of hydroxyapatite  Dissolution of minerals takes place by HCL .  Protons for acid arise from activity of cytoplasmic carbonic anhydrase 2 synthesized by osteoclasts .  Protons are released across ruffled border by a proton pump to resorption site. 55

56.  After resorption these organic and non organic particles of bone matrix are endocytosed into osteoclasts.  They are packed into membrane bound vesicles and released by exocytosis through FSD ( functional secretory domain ).  Following resorption osteoclasts undergo apoptosis which is facilitated by TGF β and estrogen. 56

57. TRAP- Tartrate resistant acid phosphatase  Active enzyme which plays an important role in bone resorption both inside and outside osteoclast cell. 57

58. RE M OD E LING OF BONE  Major pathway of bony changes in shape, resistance to forces, repair of wounds.  Regulates calcium and phosphate homeostasis  Bone remodeling involves the co-ordination of activities of cells the osteoblast and the Osteoclast. 58

59. Osteoblasts Stimulated by parathyroid hormone Release interleukin -1 and interleukin -6 Leads to migration of monocyte into bone area LIF(leukemia inhibiting factor) coalesces to form multinucleated Osteoclasts Resorbs bone and releases hydroxyapatite into the blood 59

60. Feedback mechanism Release of osteogenic substrate Differentiation of osteoblast Deposition of bone 60

61. PHASES OF REMODELING : 1. Activation phase : Stimuli such as-  Micro-fracture,  Alteration of mechanical loading  Insulin growth factor-I (IGFI)  Tumor necrosis factor-α (TNF-α)  Parathyroid hormone (PTH)  Interleukin-6 (IL-6) activate lining cells  RANKL/ RANK interaction triggers pre-osteoclasts fusion and differentiation toward multinucleated osteoclasts 61

62. 2. Resorption phase :   Once differentiated, osteoclasts adhere to the bone surface and begin to dissolve bone. They resorb the haversian lamellae and a part of the circumferential lamellae and form a resorption tunnel or cutting cone. This function requires two steps: Acidification of the bone matrix to dissolve the inorganic component Release of enzymes such as cathepsins K and MMP Osteoclasts undergo to apoptosis . 62

63. 3. Reversal phase :  After removal of debris produced during matrix degradation, osteoclasts are replaced by osteoblasts . 4. Formation phase:  Bone matrix resorption leads to the release of several growth factors:  Bone morphogenetic proteins (BMPs)  Fibroblast growth factors (FGFs)  Transforming growth factor β (TGF β)  Recruitment of the osteoblasts in the reabsorbed area  Osteoblasts produce the new bone matrix 63

64. The entire area of osteon where active formation occurs is termed the filling cone . The osteoblasts get entrapped in the new bone and are called osteocytes . Thus completing the bone remodeling process . 64

65. VITAMINS NEEDED FOR BONE REMODELLING  Several vitamins like vitamins D, C, A, and B12, play a role in bone remodeling .  The most active form of vitamin D is calcitriol. Acting as a hormone, it promotes removal of calcium from bone . On the other hand, it retards calcium loss in urine, which makes it available for deposit in bone matrix.  Vit C deficiency causes decrease collagen production, which retards bone growth and delays fracture healing . 65

66.  Vit A helps to control the activity , distribution, and co-ordination of osteoblasts and osteoclasts during development. Its deficiency results in a decreased rate of growth in the skeleton .  Vit B12 may play a role in osteoblast activity . 66

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70. More alveolar support, and less variability in periodontal support is seen in orthodontically untreated teeth than the orthodontically treated group. Proximal bone support was statistically less in all teeth measured in the treated group. The most marked alveolar differences were interproximally for maxillary and mandibular permanent incisors, and at the pressure side of closed first premolar extraction sites. 70

71. EFFECT OF EXTRACTION ON ALVEOLAR BONE 71 After multiple tooth extractions and the use of complete removable prostheses, the alveolar ridge undergoes marked contraction in both vertical and horizontal directions. Following several years of full denture use, individuals may undergo a wide variation in alveolar ridge reduction and some may exhibit a fully resorbed alveolar ridge. Single-tooth extraction, the ridge exhibits a limited reduction in its vertical dimension, but the horizontal reduction is substantial. It can be expected that: ( i ) up to 50% reduction of the original ridge width will occur; (ii) the amount of bone resorption will be greater at the buccal aspect than at its lingual/palatal counterpart; and (iii) a larger amount of alveolar bone reduction will take place in the molar regions.

72. SOCKET HEALING 72 Socket-healing process may be divided into three sequential, and frequently overlapping, phases: Inflammatory; proliferative; and modeling/remodeling.

73. 73 Inflammatory phase: The inflammatory phase may be subdivided into two parts: blood clot formation and inflammatory cell migration . The combination of inflammatory cells, vascular sprouts and immature fibroblasts forms the granulation tissue. As the site becomes sterilized, the granulation tissue is gradually replaced with a provisional connective tissue matrix that is rich in collagen fibers and cells, and the proliferative phase of the wound-healing process begins .

74. 74 Proliferative phase: The proliferative phase may also be divided into two parts – fibroplasia and woven bone formation – and is characterized by intense and rapid tissue formation . The primary osteons may be occasionally reinforced by parallel-fibered bone. Woven bone can be identified in the healing socket as early as 2 weeks after tooth extraction and remains in the wound for several weeks. Woven bone is a provisional type of bone without any load-bearing capacity and therefore needs to be replaced with mature bone types (lamellar bone and bone marrow).

75. 75 The complete remodeling of the woven bone into lamellar bone and bone marrow may take several months or years. A few weeks after tooth removal, osteoclasts could be found around the crest of both buccal and lingual walls and on the outer and inner (bundle bone) portions of the socket. Bone modeling takes place equally on buccal and lingual walls, but because the lingual bone is usually wider than the buccal bone wall , modeling results in greater vertical bone loss at the thin buccal plate than at the wide lingual wall . In addition, bone modeling takes place earlier than bone remodeling, in such way that about two-thirds of the modeling process occurs in the first 3 months of healing . Modeling and remodeling processes during socket healing result in qualitative and quantitative changes at the edentulous site, which culminate in a reduction of the dimension of the ridge . Bone modeling and remodeling phase

76. VASCULAR SUPPLY 76

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78. NERVE SUPPLY 78

79. BONE MARROW Young bone Within cavities of spongy bone Contains cells of mesenchymal and fibroblast type . YELLOW BONE MARROW Old bone Epiphysis of long bones Accumulation of fat cells Loss of haemopoetic potential  RED BONE MARROW 79

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81. Conditions involving loss of alveolar bone  The various causes of alveolar bone loss are: Extension of gingival inflammation Trauma from occlusion Systemic factors Other factors : Periodontitis Periodontal abscess Food impaction Overhanging restoration Adjacent tooth extraction Ill-fitting prosthesis 81

82. BONE DESTRUCTION CAUSED BY EXTENTION OF GINGIVAL INFLAMMATION  Most common cause of bone loss in periodontal disease is extension of inflammation from marginal gingiva into supporting periodontal tissues.  Spread of inflammation from gingiva directly to PDL is less frequent.  The transition from gingivitis to periodontitis is associated with changes in compostion of bacterial plaque.  In advanced stages number of motile organisms and spirochetes increases. 82

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84. TRAUMA FROM OCCLUSION  when occlusal forces exceeds the adaptive capacity of the tissue injury results .Trauma from occlusion;  1) ACUTE TRAUMA FROM OCCLUSION  2) CHRONIC TRAUMA FROM OCCLUSION  PRIMARY TRAUMA FROM OCCLUSION : Alteration in occlusal forces with normal periodontium with normal height of bone.  SECONDARY TRAUMA FROM OCCLUSION : Due to reduced ability of tissues to resist forces . 84

85. Bone Destruction by Systemic Disease  Osteomalacia  Diabetes;  Hyperpa r athy r oidism  Paget’s disease  Fibrous dysplasia  Osteoporosis  Osteopetrosis 85

86. 86 OSTEOMALACIA Contain a normal collagen matrix and osteoid structure, but lack proper mineralization, resulting in the softening of bones . OSTEOMALACIA OSTEOPTETROSIS Alters bone as it is developing Weakens bones that have already formed Despite the increase in bone density, the newly formed bone is of poor quality and symptoms include increased fracture incidence, neuropathy, and short stature.

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89. OSTEOPOROSIS 89 It is characterized by both alterations in the macro and microarchitecture of the bone. Multiple etiologies of this systemic disease: postmenopausal, age‐associated, glucocorticoid‐induced, secondary to cancer, androgen ablation, and aromatase inhibitors. All forms result in reduced bone strength and increased fracture risk , accompanied by a high degree of morbidity and mortality. Rapid loss of trabecular BMD and, to a lesser extent, cortical loss are common in this condition.

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93. 93 There is a pronounced increase in BMD due to abnormal bone turnover, and in some ways this is the opposite of osteoporosis. These conditions are inherited and the mode of transmission varies from autosomal dominant to autosomal recessive. It is due to a variety of defects in osteoclastic bone resorption. These include higher or lower osteoclast numbers, impaired differentiation, deficiencies in carbonic anhydrase, the ability to form a ruffled border, and alterations in signaling pathways In most cases, it is the ability of the osteoclast to create an acidic environment in the lacunae to resorb bone that is in some way compromised, ultimately resulting in a net increase in bone formation. OSTEOPETROSIS

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96. 96 Primary hyperparathyroidism is most commonly caused by a parathyroid gland adenoma. Secondary hyperparathyroidism occurs when PTH production is overstimulated in response to low serum calcium. The clinical presentation is very similar to that of rickets. Treatment includes identifying and eliminating the initiating cause.

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98. Decreased production of insulin R educe in growth P roliferation and matrix synthesis B y gingival and periodontal fibroblast and osteoblast. 98

99. FIBROUS DYSPLASIA  Localized change in normal bone metabolism leads to replacement of all components of cancellous bone by fibrous tissue containing varying amounts of abnormal bone.  Enlargement of the area with gradual blending of cortical borders.  Trabecular bone may show mixed radiolucent and radiopaque areas.  Trabeculae are shorter, thinner, irregularly shaped and more numerous than normal.(Ground glass appearance). 99

100. PAGET’S DISEASE  Abnormal resorption and apposition of osseous tissue in one or more bones.  Intense wave of osteoclastic activity with resorption of normal bone resulting in irregularly shaped resorption cavities followed by increased osteoblastic activity forming woven bone. 100

101. 3 stages- Early radiolucent resorptive stage; 2.Granular or ground glass stage and 3.Denser more radiopaque appositional stage.  Trabeculae are long, horizontal ,linearly or short and randomly arranged.  Cortical bone appears laminated. Abnormal laminadura and hypercementosis is seen. 101

102. 102 Classification of remaining bone Based on the volume of remaining mineralized bone, the edentulous sites may, according to Lekholm and Zarb (1985), be classified into five different groups. Remaining bone in the edentulous ridge

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104. 104 Peri‐implant mucositis : The presence of an inflammatory lesion in the peri‐implant mucosa and the absence of loss of supporting bone are the two fundamental features of peri‐implant mucositis. The lesion occupies a connective tissue zone lateral, but not apical, of the pocket epithelium.

105. 105 Peri‐implantitis It is a plaque‐associated pathological condition occurring in tissues around dental implants. Characterized by inflammation in the peri‐implant mucosa and subsequent progressive loss of peri‐implant bone.

106. 106 Socket housing is a three-dimensional structure, pressure/tension areas are not clearly defined and will occur simultaneously around the root, usually following a biphasic process with two concomitant sequential phases occurring in the alveolar bone. ORTHODONTIC TOOTH MOVEMENT AND BONE RESORPTION

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108. 108 Application of light mechanical forces (approximately 50–100g/tooth) on the pressure side is associated with “direct bone resorption”. In these situations, the vessels are patent, and the physiology of the cells and tissues is preserved. Stronger mechanical forces will cause a crushing injury to PDL tissues, with cell death, hyalinization, and the formation of cell-free areas between the PDL and the adjacent alveolar bone, which will interfere with the tooth movement and will slow the biologic processes.

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110. 110 Horizontal bone loss: Most common pattern of bone loss in periodontal disease. The bone is reduced in height, but the bone margin remains approximately perpendicular to the tooth surface. The interdental septa and the facial and lingual plates are affected but not necessarily to an equal degree around the same tooth. Bone destruction patterns in periodontal disease

111. 111 Vertical or angular defects They occur in an oblique direction, leaving a hollowed-out trough in the bone alongside the root. In most instances, angular defects have accompanying infrabony periodontal pockets; infrabony pockets.

112. 112 Goldman and Cohen classified angular defects on the basis of the number of osseous walls: The continuous defects that involve more than one surface of a tooth, in a shape is similar to trough, are called circumferential defects.

113. 113 BONE GRAFT It refers to a procedure where the surgeon places a bone where the positioned implant helps establish a thicker area to support it. INDICATIONS: Provide Buttress Metaphyseal Impaction Replace Bone Improved Fracture Healing

114. 114 AUTO BONE GRAFT

115. 115 ALLOGRAFTS

116. 116 SYNTHETIC BONE GRAFT

117. 117 XENOGRAFTS

118. CONCLUSION  Alveolar bone is in interdependence with the dentition.  It has a specialized function in the support of teeth.  There are architectural specifications for alveolar bone that relate to its functional role. The basic cellular and matrix components are consistent with other bone tissues. 118

119. REFERENCES Orban’s oral histology and embryology 12 th edition Ten kates oral histology 6 th edition Carranza’s Clinical Periodontology, 10 th edition. The effect of extraction and orthodontic treatment on dentoalveolar support. Alveolar socket healing: what can we learn? MAURICIO G. AR AUJO , CLEV ER SON O. SILVA, MON ICA ^ MISAWA & FLAVIA SUKEKAV 119

120. MISCH’S Contemporary Implant Dentistry Lindhe's Clinical Periodontology and Implant Dentistry 120

121. THANK YOU 121