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Oral Histology > Craniofacial bone tissues > Flashcards

Craniofacial bone tissues Flashcards

1
Q

Composition of Bones

A
  1. Inorganic (67%)
  2. Organic (33%)
    1. Collagen (28% [85% of organic])
    2. Noncollagenous proteins (5% [15% of organic])
  3. Older bones are more mineralized
  4. Osteopetrosis - very dense bone; too much mineral; Osteopetrosis can cause bones to dissolve and break
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2
Q

Bone function

A
  1. General bone functions:
    1. Mechanicl support (part of the musculoskeletal system)
    2. Ion (calcium) storage
    3. Locomotion/mastication
    4. Protection
    5. Some endocrine function controlloing homeostasis of calcium and phosphate
  2. Functions of the Alveolar process:
    1. Provides anchorage for the teeth
    2. Protects the blood nerve and lymphatic supply to the periodontal ligament
  3. Female body during pregnancy tend to lose Ca and decay of teeth too
  4. Decrease in the Ca level and phosphate content in saliva leads to decrease in teeth structure since saliva is our remineralizing element
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3
Q

Seven hierarchical levels of bone organization

A
  1. Major components/Mineral crystals
  2. Mineralized collagen fibril
  3. Fibril array
  4. Fibril array patterns
  5. Cylindrical motifs: Osteons
  6. Spongy vs Compact bone
  7. Whole bone
  • Mineralized collagen fibril is the basic building block of bone and dentin
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4
Q

Bone histology

A
  1. Mandibular bone comprises
    1. Dense compact bone
    2. Spongy trabecular bone
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5
Q

Types of bone tissues

A
  1. Different types of bone tissues, based on the organization of mineralized collagen fibrils:
    1. Parallel lamellar bone
      1. Very isotropic (same in all direction)
      2. Only good for force directed perpendicullary; potential for snapping
      3. Composed of concentric lamellae, interstitial lamellae, and circumferential lamellae (facing outside toward muscles and etc.)
        1. Osteoclast remove unncessary bones and later concentric lamellae/osteon are put in place –> remodelling
      4. The major type of human bone
    2. Woven Bone
      1. Embryonic/reparative
      2. Fast forming
      3. Poor mechanical properties
      4. During the first phase of wound healing
      5. Comprised of randomly oriented collagen fibrils
      6. Mechanically weakest
    3. Cortical Osteonal Bone (rotated plywood)
      1. Do well in any directional forces
    4. Dentin (specialized member of bone family)
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6
Q

Overall lamellar bone histology

A
  1. Lamellar bone is the primary bone type in humans
  2. Lamellae - the basic structural blocks of lamellar bone
  3. Periosteum - connective tissue membrane surrounding bone
  4. Haversian system is a primary osteon where nutrient supply is transported through
  5. Secondary osteons are remodelled
  6. Osteonal bone is produced by remodeling of circumferential lamellae
  7. Osteon - major structural unit of lamellar bone
    1. Osteons are arranged in layers of lamellae
      1. The big hole in the middle is haversian canal and osteon is refererring to the entire structure
    2. Cylindrical structure made of lamellar bone
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7
Q

Bone formation

A
  1. Intramembraneous (dermal) and endochondrial
  2. Facial and cranial vault bones form intramembraneously
  3. Skull base bones and nasal region form endocondrially
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8
Q

Endocondrial ossification

A
  1. Endochondrial ossification in long bones:
    1. Chondrocytes at the center of the growing cartilage model enlarge and die as the matrix calcifies
    2. Newly derived osteoblasts cover the shafte of the cartilage in a thin layer of bone
    3. Blood vessels penetrate the cartilage. New osteoblasts form a primary ossification center
    4. The bone of the shaft thickens, and the cartilage near each epiphysis is replaced by shafts of bone
    5. Blood vessels invade the epiphyses and osteoblasts form secondary centers of ossification
  2. Endochondrial ossification occurs on the surface of calcified cartilage
  3. Epiphyseal plate: cartilage calficiation followed by bone deposition/remodeling
    1. Reserve chondrocytes (stem-cell like) - slow proliferating pluripotent cells
    2. Cells differentiate and differentiate and eventually also get mineralized
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9
Q

Mineralization of cartilage

A
  1. Mineralization of cartilage occurs via matrix vesicles
    1. Cartilage is collagen Type 2
    2. Initial mineralization takes place via matrix vesicles
    3. Matrix vesicles are also found in different locations and around Type I, etc.
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10
Q

Intramembranous (Dermal) Ossification

A
  1. Found in craniofacial bones (neural crest origin)
  2. Ossification occurs in multiple sites of mesenchymal condensation which eventually fuse to form a continuous structure
  3. Bone formation:
    1. Coarse, woven bone. The bone is cellular and disorganized
    2. Immature bone. The bone is less cellular and slightly more organized; some primary osteons are forming
    3. Mature lamellar bone. The tightly packed osteons create an organized bone matrix; fewer cells and little connective tissue are apparent. As remodeling of the bone in its mature state takes place, the periosteal bone surface becomes more regular and eventually will be covered with circumferential lamellae.
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11
Q

Types of bone cells

A
  1. Unlike other mineralized tissues, bones constantly remodel, i.e. some of the areas are resorted and new bone is deposited. Hence new bone cells constantly differentiate
  2. Osteoblast - bone forming cells
  3. Osteocytes - bone maintenance; homeostasis
  4. Osteoclasts - removal of old bone
  5. Osteoblasts and osteocytes come from the same lineage of multipotenet mesenchymal cells
  6. Osteoclasts originate from hematopoetic precursor cells
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12
Q

Regulation of bone cell formation

A
  1. Many cells recruited; need to differentiate
    1. Bone-forming cells of mesenchymal origin
    2. Osteoclasts of hematopoietic origin
  2. Cytokines, growth factors, hormones induce cell differentiation
    1. Runx2: “Master switch,” regulates activation and repression of osteoblast growth; triggers the expression of major bone matrix proteins such as BSP, osteopontin, osteocalcin, and collagen type I, and it seems to control the maturation of osteoblasts and their transition into osteocytes
    2. Osterix: directs precursor cells into osteoblastic lineage; Osterix may play an important role in directing precursor cells away from the chondrocyte lineage and toward osteoblast lineage.
    3. Wnt pathway: beta-catenin, BMP-2
    4. Others: Dlx, Msx
  3. Multipotent mesenchyme stem cells reside primarily in the bone marrow (perivascular in craniofacial region)
    1. Terminal differentiation of osteoblasts lead to osteocytes although other just apoptose
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13
Q

Signaling pathways involved in cytodifferentiation of different bone cell types

A
  1. Runx-2 induce differentiation of mesenchymal stem cells into preosteoblast
  2. Osterix & B-catenin induce differentiation of preosteoblast into osteoblasts, which then differentiate into bone-lining cell or osteocyte
  3. M-CSF signaling molecule induce differentiation of Hematopoietic stem cell into Osteoclast progenitor, which differentiate into preosteoclast.
  4. The signaling pathway implicating the receptor-activated nuclear factor κB (RANK) and its ligand (RANKL) plays a major role in controlling osteoclastogenesis.
  5. RANKL, expressed on the plasma membrane of stromal and osteoblastic cells, binds to *RANK * expressed on the plasma membrane of osteoclast progenitors to induce a signaling cascade leading to the differentiation and fusion of osteoclast precursor cells and the promotion of the survival and activity of mature osteoclasts.
  6. Other signaling molecules/transcription factors:
    1. BMP - bone morphogenetic protein
    2. FGF - fibroblast growth factor
    3. OPG - osteoprotegerin
    4. Runx-2 - Runt-related transcription factor 2
    5. M-CSF - macrophage cology stimulating factor
    6. TRAP - tartrate resistant acid phosphatase
      1. Used by osteoclasts and thus exploited in order to detect their presence
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14
Q

Osteoblast & Osteocytes

A
  1. Osteoblast deposit bone matrix and induce its mineralization
  2. They originate from multipotent mesenchymal stem cells
  3. Osteoblasts are not terminally differentiated cells; some of them can differentiate into osteocytes
  4. Osteoblast differentiation is a highly regulated process
    1. Transcription factors activate number of seconday messengers which induce homeobox genes which lead to many different physiological changes
  5. Osteoblasts deposit mineralizing matrix
    1. Osteoid is non-mineralized proximal bone layer similr to predentin
    2. rER and Golgi are well developed in osteoblasts secreting mineralized materials
  6. Mature osteoblasts can either differentiate into osteocytes or undergo apoptosis
  7. Osteocytes recide inside the bone tissue and form numerous processes forming a 3D network:
    1. Osteocyte lacunae in osteonal bone
    2. Each of these cells have numerous processes and connect them to each other
  8. Osteocytes undergo major morphological changes where mature osteocytes have a much smaller secretory apparatus than osteoblasts
    1. Osteocytes are connected to each other and to osteoblasts via cell-cell contacts, exchanging signaling molecules via gap junctions
  9. Osteocytes are involved in the regulation of bone remodeling and repair
  10. Osteocytes regulate osteoblast differentiation via Sclerostin (negative) feedback loop
    1. Sclerostin inhibit BMP and Wnt pathways that are required for osteoblast precursors to differentiate into osteoblasts
    2. Sclerostin itself is inhibited by PTH
  11. Mechanical damage to bone tissues causes damages of osteocyte network and osteocyte go through apoptosis, triggering a cascade of events leading to bone repair
    1. Micro cracks sever osteocyte network, diminishing cell communication (and decrease of sclerostin signals) thusly inducing bone resorption
    2. More and more microcracks accumulate –> osteoclasts activity & eventually to remodeling; normal cycle of bone life
    3. Our body changes our bone periodically entirely approximately every 7 years
  12. Osteocytes are important regulators of phosphate homeostasis in the body in general
    1. DMP1 and PHEX via mature osteocyte regulate FGF23 activity, which functions to clear phosphate out of the body
    2. Defect in DMP1 leads to defect in osteocyte, which lead to uncontrolled activity of FGF23 and thusly loss of phosphate in body
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15
Q

Osteoclasts

A
  1. Osteoclasts degrade bone by dissolving mineral (low pH) and proteolysis
  2. Osteoclasts are large multinucleus macrophage-like cells of hematopoietic origin and its main function is for bone degradation
  3. Howship’s lacuna is a degraded piece of bone, each housing osteoclast
  4. Adjacent to the tissue surface, the cell membrane of the osteoclast is thrown into a myriad of deep folds that form a ruffled border; this is where the actual dissolution takes place
    1. Large surface area is advantageous for increased output of bone degradation activity
  5. At the periphery of this border, the plasma membrane
    is apposed closely to the bone surface, and the adjacent cytoplasm, devoid of cell organelles, is enriched in actin, vinculin, and talin (proteins associated with integrinmediated cell adhesion). This clear or sealing zone not only attaches the cells to the mineralized surface but also (by sealing the periphery of the ruffled border) isolates a microenvironment between them and the bone surface.
  6. The enzymes are synthesized in the rough endoplasmic reticulum, transported to the Golgi
    complexes, and moved to the ruffled border in transport vesicles where they release their content into the sealed compartment adjacent to the bone surface, essentially creating an extracellular lysosome
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16
Q

Major factors involved in the regulation of Osteoclast differentiation and bone remodeling

A
  1. RANK (a receptor) presented on the membrane of preosteoclast cells
  2. RANKL (a ligand) presented on the membrane of stromal and immature osteoblastic cells
    1. RANKL is secreted by preosteoblasts
    2. Process also regulated by Wnt pathway
  3. Osteoprotegerin (OPG) is an inhibitor of osteoclast differentiation, produced by mature osteoblasts. It is soluble, binds to RANK preventing RANK-RANKL binding, thusly inhibiting osteoclast differentiation
    1. OPG is a look-alike of RANKL
    2. OPG is secreted by mature osteoblasts
  4. Osteoclasts differentiate from hematopoetic precursor cells
    1. Osteoclast differentiation is regulated by various pro- and anti-inflammatory cytokines converging on RANKL-OPG, and their net balance determines bone loss
    2. T-cells induce the generation of RANKL
    3. In periodontal disease, the bone resorption is caused by both bacterial activity and also due to immune response inducing bone resorption
  5. Cancer cells metastasizing to bone secrete factors disrupting (by secreting its own RANKL) the normal interplay between osteoclasts and osteoblasts, to favor an osteolytic response and allow metastasizing cells to propagate
17
Q

Bone remodeling cycle

A
  1. Bone remodeling depends on differentiation of osteoclasts and osteoblasts
  2. Bone growth is a remodeling process and our bones completely remodel every 7-10 years; new bone deposition on the outside, and resorption in the inside
  3. The process occurs through the cooperative activity of various cells that form a temporary functional compartment known asbasic multicellular unit or bone remodeling unit. The process begins with the activation of osteoclast formation, followed in order by
    1. A resorption phase during which osteoclasts remove old bone and create the resorption lacuna,
    2. Reversal in which mononuclear cells (macrophage-like or osteoblast precursors) deposit a cement line,
    3. A formation phase during which new bone is deposited, and finally
    4. A resting phase during which osteoblasts become quiescent and become the flattened bone lining cells.
  4. The sequence of events at these temporary and evolving anatomic sites consists of five phases: activation, resorption, reversal, formation, and resting
  5. During the resorption phase, bone is removed and a resorption lacuna is created. Factors produced by osteoclasts, mononuclear reversal cells, or liberated from the resorbed bone matrix trigger the formative phase during which the lacuna then is filled with new bone produced by osteoblasts recruited at the site.
  6. As these osteoblasts mature, they produce more osteoprotegerin and less RANKL, leading to a reduction in RANK/RANKL interactions. This results in an inhibition of osteoclast activity, thereby allowing osteoblasts to refill the resorption lacuna.
  7. The formation phase lasts substantially longer than the resorption and reversal phases together. Osteocytes are likely implicated in “sensing” the need for remodeling and transmitting signals via their extensive canalicular network to osteoclast and osteoblast compartments.
  8. The release of mineral ions during bone turnover,
    together with the concerted action of the kidneys and intestine, is an integral part of the phosphocalcic homeostatis system.
18
Q

Complications with bone remodeling cycle

A
  1. Osteoporosis - remodeling cycle imbalance can be caused by decrease in bone deposition or increase in bone resorption
    1. Treatments include Antiresorptive and Anabolic
  2. Antiresorptive
    1. Bisphosphonate based drugs interrupt osteoclast differentiation
    2. Estrogen treatment maintains osteoclast-osteoblast balance
  3. Anabolic treatment
    1. Teriparatide (Forteo) - recombinant human parathyroid hormone (PTH) fragment
    2. PTH suppresses the Sclerostin activity, which interfere with osteoblast differentiation into osteocytes; inhibition of inhibitor.
    3. PTH also causes changes in calcium homeostasis
19
Q

Osteonecrosis

A
  1. Osteonecrosis is a debilitating condition, which is caused by a poor blood supply to the area
  2. Osteonecrosis occurs when part of the bone does not get blood and dies
  3. Osteonecrosis of jaws is associated with bisphosphonate treatments, which tend to reduce bone resorption and lead to “sealing” of the vasculature
    1. These affected bones don’t regenerate since vascular bones did not get nutrition and energy needed to sustain its integrity and eventually die
20
Q

Bisphosphonate

A
  1. Bisphosphonates are structurally similar to pyrophosphate, one of the major phosphate compounds in the body
    1. Ones that contain Nitrogen in the side chains are more potent
  2. Bisphosphonates strongly bind to apatitic crytals (i.e. hydroxyapatite) due to high affinity between calcium and phsphate and reduce their solubility
    1. Reduced mineral solubility makes the bone tissue more resoprtion resilient
  3. Due to their high affinity to hydroxyapatite bisphosphonates accumulate in bone tissues hence the concentration of bisphosphonates in bone is high and constantly increasing in chronic patients
    1. High affinity BP is characterized by avid uptake, lower desorption, higher re-attachment, and less diffusion in bone; HA won’t leave
  4. Biological effects of bisphosphonates on osteoclasts
    1. Nitrogen-containing bisphosphonate disrupt certains steps along the pathways necessary for osteoclast differentiation
    2. Bisphosphonate endocytosis from the bone surface by osteoclast leads to apoptosis
21
Q

Therapeutic applications of bisphosphonates

A
  1. Used whenever there is a need to slow bone resorption
  2. Cancer treatment
    1. Tumor cells induce osteoclast activity
    2. Bisphosphonates used to slow down bone degradation by increased osteoclast activity by being taken up by OCL’s and inducing OCL apoptosis
  3. Osteoporosis treatment
    1. Osteoporosis is a bone loss due to the elevated osteoclast activity or changes in Ca2+ metabolism
22
Q

Paget’s Disease

A
  1. Abnormal bone remodeling, usually localized to isolated areas of the skeleton, chracterized by low density poor quality bone tissue, witu large amount of osteoid and slow rate of mineralization
  2. Bisphophonate treatments is beneficial for slowing down resorption
23
Q

Problems with bisphosphonates

A
  1. Effects of bisphophonates on bone tissue–> lack of remodeling leads to low vascularization of the tissue
  2. Too much bisphosphonates during cancer treatment will lead to excessive mineralization of bone and over calcification thus blood vessels will be crushed and closed and eventually become necrotic; very few osteons are observed
    1. The risk of osteonecrosis is associated primarily with cancer treatments which use much higher doses than in the osteoporosis treatments
    2. Mandible is more frequently affected than maxilla
  3. Lack of remodeling leads to devascularization and thusly to a decrease in immune response also, hence no way to fight off infection in bone
  4. Suppression of osteoclastic activity prevents removal of diseased bone
  5. Jaws are especially affected since it is more exposed to the outside environment
  6. Accumulation of micro cracks in bisphophonate treated bones, with no way of remodeling, will lead to catastrophic fracture
  7. An extended bisphosphonate antiresorptive therapy for treatment of osteoporosis (>3 years) can also lead to bisphosphonate-related osteonecrosis of the jaw (BRONJ)
  8. Clinical considerations
    1. Bisphosphonates accumulate in the body, hence no mater when a person has been treated for cancer with bisphosphonates, they have a risk of developing BRONJ
    2. Low dose long term administration of bisphosphonates might lead to osteonecrosis
    3. Patients have to complete all ncessary dental and periodontal work prior to cancer treatments to minimize the risk of bone exposure
24
Q

Composition of the bone tissues

A
  1. Carbonated apatite is the major mineral phase in bone, dentin and enamel
  2. Organic matrix composition of bone tisseus
    1. Collagen Type I is the major organic phase in bone tissues and dentin (~90%);
    2. Noncollagenous matrix proteins (SIBLING family, Osteocalcin, Osteonectin)
    3. Enzymes (MMPs, phosphotases others)
    4. Proteoglycans (mainly SLRPs)
    5. GAGs
    6. Other molecules such as phospholipids
  3. Collagen Type I
    1. Major protein of bone and dentin
    2. Mineralized collagen fibril is a basic building block of bone and dentin
    3. Essential role in mineralization and mechanical properties of bone and dentin
    4. Refer to Dentin Lectures for details
25
Q

Noncollagenous Macromolecules (Proteins)

A
  1. Proteoglycans
    1. SLRPs = Small Leucine Rich Proteoglycans (SLRPs)
    2. Decorin, Biglycan, FIbromodulin, Lumican
    3. SLRPs specifically interact with collagen molecules
    4. Horse-shoe structure that fits on top of collagen fibril; control diameter of collagen
    5. Important in cornea of the eyes as collagen much narrower
  2. Proteoglycans affect kinetics of collagen fibrilogenesis
    1. Proteoglycans decorin and lumican influence kinetics of collagen fibril formation
    2. Lumican induce fibrogenesis onset to start early
    3. Decorin delays the the onset of fibrogenesis and also underdevelopment of collagen
    4. Combination of two proteoglycans lead to yet anoter different effect on fibrogenesis
  3. Proteoglycans regulate collagen fibril shape and size
    1. Abnormal collagen fibrils in tendons of decorin knockout mouse; diameter vary significantly, amorphous mass vs in control bimodal distribution of large and small fibers
    2. Abnormal collagen fibrils in biglycan/fibromodulin knockout mouse
    3. Regenerated tendons are NOT the same as the native tendons and are not as mechanically; they tend to overcome the problem by making them larger and broader and amorphous as a consequence;
    4. SLRPs are very important in fibril assembly and diameters
26
Q

SIBLINGs

A
  1. Small Integrin Binding Ligand N-linked GLycoproteins are multifunctional proteins
    1. Mineralization
    2. Phosphate homeostasis
    3. Protect cells from lysis
    4. Other functions
    5. See dentin lecture for details on DMP1 and DSPP
  2. DSPP is also expressed in alveolar bone, cementum and condylar cartilage
    1. Loss of DSPP leads to periodontal diseases in mice
    2. Severe apical periodontitis in DSPP KO animals
    3. Less bone in these animals and cannot regenerate to the level of control animals
27
Q

Osteopontin (OPN)

A
  1. Multifunctional SIBLING glycoprotein
  2. 44 KDa, rich in Glu, Asp, and Ser, calculated pI=4.61, disordered; acidic like others
  3. Undergoes a series of post-translational modifications, i.e. phosphorylation, glycosylation, and sulfation
  4. Major sialoprotein in bone, dentin, and hypertrophic cartilage (also found in kidney, brain, blood cells, and vascular muscles)
  5. Found in high Ca2+ body fluids, i.e. urine, milk, seminal fluid and bile, where it prevents spontaneous mineral precipitation; anti-crystallization/mineralization
  6. Besides its role in mineralized tissues, it has multiple other functions:
    1. Key cytokine,
    2. Involved in tissue repair
    3. Inflammation; found in metastasizing cancers
    4. Prevent formation of kidney stones
    5. Prevent precipitation of minerals i.e. Calcium
  7. Osteopontin is found in extrafibrillar spaces
  8. OPN KO mice display:
    1. Reduction in the ovarectomy induced bone resorption
    2. Hypermineralization and higher level of mineral crystallinity; mineral to matrix ratio is higher in KO
28
Q

Bone Sialoprotein (BSP)

A
  1. Multifunctional SIBLING Glycoprotein
  2. Most Abundant SIBLING Protein of bone (15% NCPs); also expressed by odontoblasts and cementoblasts
  3. 30 KDa, Rich in Glu, Ser and Tyr, Calculated pI=4.16
  4. Undergoes a Series of Posttranslational modifications, i.e. Phosphorylation, Glycosylation and Sulfation
  5. Specifically Binds to Collagen
  6. Contains Integrin Binding Motif
  7. Promoter of Calcium Phosphate Mineralization
  8. Involved in Osteoclast Differentiation
  9. Found in Metastasizing Cancers
  10. BSP Knockout
    1. BSP regulates osteoclast activity in bone repair process
    2. Decreased bone repair and remodeling in the BSP KO
29
Q

Non-SIBLINGs Proteins

A
  1. Osteocalcin (OC, Bone Gla protein)
    1. Small Multyfunctional Protein (Proprotein is only 100AA, mature protein is 49 AA in Humans); 8 (5 in mature) Glu.
    2. Belongs to Vitamin K dependant Gla proteins
    3. Major Protein in Bone, Dentin and Cementum; also found in Blood Serum
    4. Posttranslation Modifications: Carboxylation of multiple Glu residues i.e. carboxyglutamic acid
    5. Found in Bones and Dentin, abundant at the sites of initial mineralization
    6. Strong Inhibitor of Mineralization; inhibits spontaneous mineral precipitation
    7. Other Functions: Regulation of osteoclast differentiation
  2. Osteocalcin KO mice have higher bone mass & thickness and higher rate of bone deposition, suggesting its role in the suppression of bone formation
    1. Die of complete calcification of arteries
    2. Tetracyclin staining is very good for viewing bone deposition and growth
  3. Osteonectin (SPARC)
    1. Acidic extracellular matrix protein, rich in Asp, Glu, and Cysteine (disulfide bonds). pI=4.8
    2. Found in bone, dentin as well as in many nonmineralized tissues, i.e. brain
    3. Specifically binds to collagen
    4. Its rle in mineralization is NOT clear
    5. Regulates steoblast and osteoclast activity/bone formation and remodeling
    6. Promotes cell-matrix binding
  4. Enzymes
    1. Proteinases:
      1. Specific- responsible for specific proteolytic cleavage of matrix proteins. Activate/deactivate matrix proteins (i.e. MMPs, Collagenases, PHEX)
      2. General - proteolytic degradation of protein matrices (i.e. Tripsin, Pepsin)
    2. Phosphatases:
      1. Dephosphorylate organic matrix molecules, which can lead to increase o f local phosphate concentration and induce mineralization (i.e. Alkaline Phosphatase)
    3. Kinases:
      1. Phosphorylate matrix macromolecules (i.e. Casein Kinase)
30
Q

Functions of SIBLINGS in mineralization

A
  1. Bone Sialoprotein (BSP)
    1. Rich in bone; Low in dentin
    2. Increased mineralization
    3. Decreased osteoclast differentiation
  2. Osteopontin (OPN)
    1. Rich in bone; Low in dentin
    2. Decreased mineralization
    3. Osteoclast regulation
    4. Immune response
    5. Inflamation
    6. Implicated in cancer, kidney stones, atherosclersis
  3. Dentin Matrix Protein 1 (DMP1)
    1. Rich in bone; Rich in dentin
    2. Increased mineralization
    3. Pi metabolism
    4. Implicated in hypophosphatemic rickets
  4. Dentin Sialoprotein (DSP)
    1. Medium in dentin; Rich in bone maxillofacial; Low in long bone
    2. Mineralization (unclear)
    3. Implicated in DI and Dentin dysplasia
  5. Dentin Phosphoprotein (DPP)
    1. Rich in dentin; Rich in bone maxillofacial; Low in long bone
    2. Increased mineralization
    3. Implicated in DI and Dentin dysplasia
31
Q

Functions of Non-SIBLING proteins in mineralization

A
  1. Ostecalcin (OC) - bone Gla protein
    1. Found in bone and dentin
    2. Decreased mineralization
    3. Glucose Metabolism: affects insulin release
  2. Osteonectin (ON)
    1. Found in bone
    2. Mineralization (unclear)
32
Q

Mineralization by bone cells

A
  1. Nonmieralized collagenous matrix is deposited by osteoblasts and odontoblasts, which is mineralized several microns away from the cells
  2. Matrix Vesicles are produced by osteoblasts, osteocytes, and odontoblasts
33
Q

Alveolar bone

A
  1. Cortical bone interfacing with PDL is called lamina dura, lamina cribrosa, or alveolar bone proper.
  2. Alveolar bone proper is highly perforated thusly the name lamina cribrosa; blood vessels run through these areas
  3. The bone of the mandible and maxilla consist of compact cortical plates, inner trabecular bone, and a marrow cavity
  4. The size, shape and orientation of the trabeculae depend upon functional forces.
  5. In the body of the maxilla or mandible, the configuration of the trabeculae are governed by masticatory muscles.
  6. In the alveolar processes the configuration of the trabeculae are governed by the functional activity of the teeth
  7. The high turnover rate of the alveolar bone gives it the appearance of bundle bone (dense)
  8. Fenestrations are apical defects in which a portion of the root protrudes through the cortical plate, the defect is surrounded by bone
  9. Dehiscence is a coronal defect, a portion of the root protrudes through the cortical plate, the defect is not completely surrounded by bone but is open coronally.

Oral Histology (7 decks)

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