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The bone remodeling rate (BRR): the period of time needed for new bone to replace the existing bone and to allow for the adaptation of bone to its environment BRR is expressed as a percentage or volume of new bone within a specific time period.
reversal.phases of bone remodelling • : • activation. resorption. formation and • termination. .
Scheme of origin. interactions and local factors required for differentiation/function of the osteo-cells involved in bone remodeling. .
Scheme of the interactions considered in the mathematical model describing forceinduced bone adaptation .
Cells of bone remodling • • • • • • 1-Osteoclasts 2-Osteocytes 3-Osteoblasts 4-T-cells and B-cells 5-Megakaryocytes 6-Osteomacs .
The cycle of bone remodeling Activation Resorption Reversal (cement line formation) Formation (osteoid deposition) Mineralization (osteoid mineralization) Quiescence 6 monthes 3 monthes 3 days 4 weeks (Martin et al. 1998. . pp. 80-83)..
Skeletal Remodeling .
Therefore. Such predictions can help to minimize the possibility of implantation failure. . it is • crucial to understand the magnitude and the development of mechanical stress inside the bony • tissues. bone remodelling is in • essence a process where the bone changes its own property to adapt to its changing mechanical • loading environment . This will have the effect of • reducing the rate of implant failure. where the bone density is • changed due to the implant induced mechanical loading . bone remodelling occurs. therefore • leading to the stabilization of the dental implant inside the dental bone. Therefore. in order to optimize the dental implant design. As bone remodels positively.• Concurrently with osseointegration process. the quality of the bone will improve.
mechanotransduction • The conversion of biophysical force to cellular and biochemical response • It comprises four phases • 1-mechanocoupling • 2-biochemical coupling • 3-transmision of signal from sensor to effector cells • 4-effector cell responses .
Cellular Response to Loading • Cellular functions to remodel the bone is controlled by a feedback loop: Tissue Strains Proximal Stimuli Cellular Deformation d .dmin = Ddcell Tissue Remodeling do not add bone add bone 0 Ddcell .
Cellular Mechanoreception • Cells contain specialized structures to detect mechanical stimuli: + + + + voltage activated ion channels stretch activated ion channels integrin interactions and cytoskeletal mechanisms • Most mechanoreceptors require cellular deformation to transduce the signal .
• Mechanical loading requires signaling through the Lrp5 receptor to initiate bone formation. • This signal is initiated by Wnt, which binds to the receptor complex made up of Lrp5 and • Frizzled. Wnt signaling can be blocked by Dickkopf related protein (Dkk) when it binds Lrp5 • and Kremen. Sclerostin (Sclr) inhibits Wnt signaling by binding Lrp5 and secreted • Frizzled-related protein (sFrp) binds to Wnt and prevents signaling. Each of these inhibitors • blocks mechanotransduction and reduces bone formation.
• • • • • • • • • • • • • • •
Fluid shear on osteocytes (OCY) induces an influx of
extracellular Ca2+ via voltage-sensitive (V) and perhaps mechanosensitive (M) channels. Shear stress also enhances ATP release, which binds to the purinergic receptors P2X (ionotropic) and P2Y (metabotropic). Signaling through P2Y is required for Ca2+ release from intracellular stores via a Gq – PLC – PIP2 – IP3 pathway. ATP release causes PGE2 release through signaling downstream of the P2X7 receptor. PGE2 binds and signals through one of the EP receptors, probably EP4 and/or EP2, and ultimately results in enhanced bone formation. PTH signaling also appears to be required for mechanotransduction to occur, but the intracellular pathways involved are not well understood (question mark). Wnt signaling through the Lrp5 receptor, which acts through beta catenin (β-cat) translocation to the nucleus, also appears to be important in mechanically induced bone formation. Pressure in the marrow cavity and/or fluid shear forces on marrow stromal cells (MSC) may stimulate nitric oxide synthase (NOS) activity and nitric oxide (NO) release. NO is a strong inhibitor of bone resorption and probably acts by inhibiting RANK-L expression, while increasing osteoprotegerin (OPG) production (RANK-L enhances osteoclast differentiation, whereas OPG suppresses this process). OCY = osteocyte; OB = osteoblast; MSC = marrow stromal cell.
suggesting that skeletal fragility in individuals afflicted with OPPG might be related to inadequate processing of signals derived from mechanical stimulation.• • • • • • • • Lrp5 appears to be a potent regulator of bone mass. One of the main mechanisms of action for the receptor in bone is through mechanical signaling. . and strength. Lrp5 is a late-acting mediator in the osteogenic response to mechanical loading. size. • intermittent • PTH might be an effective treatment for improving bone mass • in these patients.
Mechanotransduction in Cells • Pathways for mechanotransduction .
• • • • • • • • • • • • • • • • forces applied through the ECM (A) or directly to the cell surface (B) travel to integrin-anchored focal adhesions through matrix attachments or cytoskeletal filaments. Focal adhesion kinase (FAK) may be involved in Shc recruitment as well as modulation of Rho activity which. can regulate the force response through mDia1. PKA-c . Tal. talin) that connect directly to microfilaments and indirectly to microtubules. CD47 associates with the integrin heterodimer to form a protein complex with seven transmembrane segments that mimics the action of G protein-coupled receptors. Internally-generated tension and forces transmitted through cell-cell contact similarly reach focal adhesions through the cytoskeleton. when integrins are mechanically stressed. the complex stimulates Gs-mediated up-regulation of the cAMP cascade through adenylate cyclase (AC). in turn. vinculin. Forces concentrated within the focal adhesion (magnified at bottom of figure) can stimulate integrin clustering and induce recruitment of additional cytoskeletal linker proteins (Vin. resulting in nuclear translocation of the catalytic subunit of protein kinase A. respectively. Caveolin-1 (cav-1) can also recruit Shc to integrins to activate the ERK cascade. Pax. paxillin. Forces applied to this specialized cytoskeletal adhesion complex also activate integrin-associated signal cascades. In the case shown.
Factors affecting bone modling and remodling around dental implant .
The results suggested that implant loading might have significantly affected the responses of periimplant osseous structures. Among the three remaining implants.5 months of loading (Isidor 1996. 1997). it should be noted that the loss of osseointegration observed might have been attributed to the unrealistically high-occlusal overload used in the study . it was observed that five out of eight implants lost osseointegration due to excessive occlusal overloading after 4. one showed severe crestal bone loss and the other two showed the highest bone– implant contact and density.In non-human primate studies. However.5–15.
If such loading regimens could be applied for dental implants. anabolic effects on bone. a favorable mechanical environment for osseointegration is promoted. Bone-implant interface maturation could be faster because bone deposition increases. Low-magnitude high frequency (30-50 Hz) mechanical signals produce. instead.• • • • • • • • • • • Low-amplitude and low frequency specific strains (15-30 Hz) were demonstrated to have an osteogenic effect and act as a growth factor to encourage bone response to loading (19). .
Mechanotransduction pathways shown to be involved in the mechanical response of osteoblastic cells .
Local Regulation of Bone Healing Growth factors Cytokines Prostaglandins/Leukotrienes Hormones Growth factor antagonists .
This is the rationale for the use of conservative surgical approaches in these procedures. The surgery-induced trauma can be highly detrimental for the release of a flap and induces some cell death. the more bone resorption occurs. . The more the bone is exposed and dried by suction. which provokes an inflammatory process and brings mediators of bone resorption.• • • • • • • • Preserving the Bone Level Marginal bone remodeling is obviously a multifactorial issue.
• the respect of the mucosal seal is essential to prevent bone • remodeling and soft tissue aesthetic repercussions.
• The transmucosal components‟ • design should be concave, inwardly narrowed in order to • positively impact the soft tissues
• The mobility of the peri-implant mucosa is highly deleterious • because when tearing of connective tissue occurs with • microbleeding, the protective role of the junctional epithelium • induces the apicalization of the latter. By consequence, a layer • of connective tissue of 1mm (in average) has to reform more • apically – often at the expense of the bone crest
• • • • • • Growth Factors Transforming growth factor Bone morphogenetic proteins Fibroblast growth factors Platelet-derived growth factors Insulin-like growth factors .
osteoclasts and chondrocytes • Stimulates both endochondral and intramembranous bone formation – Induces synthesis of cartilage-specific proteoglycans and type II collagen – Stimulates collagen synthesis by osteoblasts .• Transforming Growth Factor • Superfamily of growth factors (~34 members) • Act on serine/threonine kinase cell wall receptors • Promotes proliferation and differentiation of mesenchymal precursors for osteoblasts.
• Bone Morphogenetic Proteins • Osteoinductive proteins initially isolated from demineralized bone matrix – Proven by bone formation in heterotopic muscle pouch • Induce cell differentiation – BMP-3 (osteogenin) is an extremely potent inducer of mesenchymal tissue differentiation into bone • Promote endochondral ossification – BMP-2 and BMP-7 induce endochondral bone formation in segmental defects • Regulate extracellular matrix production – BMP-1 is an enzyme that cleaves the carboxy termini of procollagens I. II and III .
6.• Bone Morphogenetic Proteins • These are included in the TGF-β family – Except BMP-1 • BMP2-7. & 9 may be the most potent in osteoblastic differentiation • Work through the intracellular Smad pathway • Follow a dose/response ratio .9 are osteoinductive • BMP2.
Timing and function of growth factor .
• BMP Antagonists • May have important role in bone formation • Noggin – Extra-cellular inhibitor – Competes with BMP-2 for receptors .
• BMP Future Directions • BMP-2 – Increased fusion rate in spinal fusion • BMP-7 equally effective as ICBG in nonunions • Must be applied locally because of rapid systemic clearance • ? Effectiveness in acute fractures • ? Increased wound healing in open injuries • Protein therapy vs. gene therapy .
then one can control bone remodeling through mechanical stress that applied through exercise either voluntarily or with the help of mechanical devices.Importance of mechanical aspects If we know the mechanical aspect well. (orthopedics) .
• Fibroblast Growth Factors • Both acidic (FGF-1) and basic (FGF-2) forms • Increase proliferation of chondrocytes and osteoblasts • Enhance callus formation • FGF-2 stimulates angiogenesis .
PDGF-A and PDGF-B – PDGF-BB and PDGF-AB are the predominant forms found in the circulation • Stimulates bone cell growth • Mitogen for cells of mesenchymal origin • Increases type I collagen synthesis by increasing the number of osteoblasts • PDGF-BB stimulates bone resorption by increasing the number of osteoclasts .• Platelet-Derived Growth Factor • A dimer of the products of two genes.
• Insulin-like Growth Factor • Two types: IGF-I and IGF-II – Synthesized by multiple tissues – IGF-I production in the liver is stimulated by Growth Hormone • Stimulates bone collagen and matrix synthesis • Stimulates replication of osteoblasts • Inhibits bone collagen degradation .
macrophage and granulocyte/macrophage (GM) colony-stimulating factors (CSFs) and Tumor Necrosis Factor • Stimulate bone resorption – IL-1 is the most potent • IL-1 and IL-6 synthesis is decreased by estrogen – May be mechanism for post-menopausal bone resorption • Peak during 1st 24 hours then again during remodeling • Regulate endochondral bone formation .• Cytokines • Interleukin-1.-6.-11.-4.
Specific Factor Stimulation of Osteoblasts and Osteoclasts • Osteoclasts Cytokine Resorption IL-1 TNF-α TNF-β TGF-α TGF-β PDGF IGF-1 IGF-2 FGF Bone Formation + + + -++ ++ +++ +++ +++ Bone +++ +++ +++ +++ ++ ++ 0 0 0 .
• Prostaglandins / Leukotrienes • Effect on bone resorption is species dependent and their overall effects in humans unknown • Prostaglandins of the E series – Stimulate osteoblastic bone formation – Inhibit activity of isolated osteoclasts • Leukotrienes – Stimulate osteoblastic bone formation – Enhance the capacity of isolated osteoclasts to form resorption pits .
• Vascular Factors • Metalloproteinases – Degrade cartilage and bones to allow invasion of vessels • Angiogenic factors – Vascular-endothelial growth factors • Mediate neo-angiogenesis & endothelial-cell specific mitogens – Angiopoietin (1&2) • Regulate formation of larger vessels and branches .
++ moderately similar. +++ most similar. Canine Macrostructure Microstructure Bone Composition Bone Remodelling ++ ++ +++ ++ Sheep/Goat Pig +++ + ++ ++ ++ ++ +++ +++ Rabbit + + ++ + + least similar. Summary of four key attributes in terms of similarity between animal and human bone. .species • Table 1.
Signficans of bone remodling • responsible for removal and repair of damaged • bone to maintain integrity of the adult skeleton • and mineral homeostasis. .
htm .Bone Remodeling • Bone structural integrity is continually maintained by remodeling – – – Osteoclasts and osteoblasts assemble into Basic Multicellular Units (BMUs) Bone is completely remodeled in approximately 3 years Amount of old bone removed equals new bone formed http://www.elixirindustry.com/resource/osteoporosis/jilka.
• • • . A. Currently available bone biochemical markers. Resorption Urine – – – – – Hydroxyproline Free and total pyridinoline (Pyd) Free and total deoxypyridinoline (Dpd) N-telopeptide of collagen cross links (NTx) C-telopeptide of collagen cross links (CTx) • Serum – – – – Cross-linked C-telopeptide of type I collagen (ICTP) Tartrate-resistant acid phosphatase (TRAP) NTx CTx . Formation Serum – – – – Bone specific alkaline phosphatase (BSAP) Osteocalcin Carboxy-terminal propeptide of type I collagen (PICP) Amino-terminal propeptide of type I collagen (PINP • • B..
htm Osteocytes Activation Quiescence Resorption Formation & Mineralization Reversal .org/ejifcc/ vol13no4/130401004n.ifcc.BMU Remodeling Sequence www.
tissue growth) – ACH (adrenal-cortical hormone) : decreases cell division & subsidiary processes. affect cartilage & lamellar bone. C & D & calcitonin . – T4 (thyroxine): affects all tissues.• Endocrine – STH (somatotropic or growth hormone): increases cell division & all subsidiary processes (total protein synthesis. – Estrogens: selectively decrease cell division & subsidiary processes. net protein synthesis. total turnover. – Vitamins A.
6. • Biochemical activity of calcium – Straining bone increases calcium concentration in interstitial fluid – Change in solubility of HA crystals in response to stress .12.2 Mechanism for control of remodeling • Piezoelectricity – Mechanism for bone to sense stress & cause remodeling – Collagen – Electrical field is capable of activating proteinsynthesizing organelles in osteogenic cells (frog). Electrical field cause tropocollagen alignment.
net loss of bone calcium & phosphorous. radiographic opacity & size. after resume of normal activity mineral loss phenomena reversed ! • Astronauts subjected to weightlessness has same results: subnormal stresses causes loss of bone strength. Rigid plate fixation in dog yields thinning of femoral diaphysis cortex rather than osteoporosis . • Intermittent stress is a morphogenetic stimulus to functional adaptation of bone & effect of compressive stress is same as tensile stress ! • Distribution of material & strength is related to severity of stress in normal activity.Stress-controlled bone development • Compressive stress stimulates formation of new bone and important factor in fracture healing • During immobilization.
in bodily fluids – Bones are remodeled in response to the mechanical stress it experiences • Osteons of compact bone and the trabeculae of spongy bone are constantly replaced by new osteons and trabeculae that are more precisely aligned with newly experienced compressive and tensile forces .Bone Remodeling • Bone of the skeleton are continually remodeled for 2 reasons – Bone remodeling helps maintain constant concentrations of Ca2+ and PO43.
Inc.Factors Affecting Bone Growth and Bone Remodeling • Normal bone metabolism depends on several factors – Minerals • Large amounts of calcium and phosphorus and smaller amounts of magnesium. John Wiley & Sons. and manganese are required for bone growth and remodeling – Vitamins • Vitamin A stimulates activity of osteoblasts • Vitamin C is needed for synthesis of collagen • Vitamin D helps build bone by increasing the absorption of calcium from foods in the gastrointestinal tract into the blood • Vitamins K and B12 are needed for synthesis of bone proteins Copyright 2009. 64 . fluoride.
increased interface • strength. superior stability and osseous adaptation at • the bone/implant interface in the simvastatintreated • group3 .medications • Simvastatin is a lipid lowering agent with osteoanabolic • effects. Histomorphometric studies have shown increased • bone ingrowth and mechanical examination.
– A decrease in bone mass occurs.Aging and Bone Tissue • The level of sex hormones diminishes during middle age. 66 . Inc. – Bone resorption by osteoclasts outpaces bone deposition by osteoblasts. • Female bones generally are smaller and less massive than males. John Wiley & Sons. Copyright 2009. especially in women after menopause. – Loss of bone mass in old age has a greater adverse effect in females.
3-D Micro CT: Healthy vs Osteoporotic Bone .
89- .• Bisphosphonates inhibit osteoclast-mediated bone • resorption and normalize the high rate of bone turnover that • characterizes osteoporosis.62. there is a rationale • for using bisphosphonates to enhance early stability of • implants in patients with low bone mass30. Consequently.
but it • does not seem to significantly affect longterm osseointegration • of porous-coated implants98.• indomethacin causes a transient • decrease in attachment strength at early periods. .
• dalteparin and unfractionated heparin led to a significant • decrease of matrix collagen type II content and calcification • in concentrations equal or higher than the therapeutic one.• warfarin. . Enoxaparin.
01-100 جg/ml). a synthetic anticoagulant substance • similar to heparin. fondaparinux may • be used to avoid the heparin-related negative influence on • osteoblast-dependent fracture healing and endoprosthetic • implant integration99. showed no inhibitory in vitro • effects on human osteoblasts within the concentration range • investigated (0.100.• fondaparinux. . Therefore.
.• radiation therapy seems to delay bone remodeling preand • post-implantation35.
• Recently. Direct application • of the BMP-2 gene using a liposomal vector enhanced • bone regeneration in a bony defect. gene delivery combined • with bone grafting could induce rapid osseointegration of • the bone-implant interface at an earlier stage121. cell-mediated regional • gene therapy was introduced to deliver potent morphogens • or growth factors in regenerative medicine. .
Aging and Bone Tissue • There are two principal effects of aging on bone tissue: – Loss of bone mass • Results from the loss of calcium from bone matrix • The loss of calcium from bones is one of the symptoms in osteoporosis – Brittleness • Results from a decreased rate of protein synthesis • Collagen fibers give bone its tensile strength • The loss of tensile strength causes the bones to become very brittle and susceptible to fracture Copyright 2009. John Wiley & Sons. Inc. 74 .
• Meloxicam negatively • influenced bone healing in the cortical and cancellous • bone around titanium implants inserted in rats after continuous • administration .
76 .Aging and Bone Tissue • Osteoporosis – Condition where bone resorption outpaces bone deposition – May be due to depletion of calcium from the body Copyright 2009. Inc. John Wiley & Sons.
Histology of Bone Tissue Copyright 2009. 77 . Inc. John Wiley & Sons.
endosteum.Bone Remodeling • Bone forming osteoblasts form from mesenchyme-like stem cells located in the periosteum. and the connective tissue of nearby bone marrow • Osteoclasts form in bone marrow from immature blood cells called hematopoietic stem cells • Many of these stem cells fuse together to form each osteoclast. thus their multinucleate structure .
osteoclasts take up collagen and dead osteocytes by phagocytosis .Bone Remodeling • Osteoclasts release calcium ions (Ca2+) and phosphate ions (PO43-) that enters the tissue fluid and the bloodstream • Lysosomal enzymes are also released by the osteoclasts and digest the organic part of the bone matrix • Finally.
Bone Remodeling • The ruffled plasma membrane forms a tight seal against the bone and HCL dissolves the mineral portion of the matrix .
Bone Remodeling • Osteoclasts are large cells with many nuclei • Their plasma membrane is highly folded or ruffled .
Bone Remodeling • Bone remodeling is coordinated by cohorts of adjacent osteoclasts called remodeling units • Osteoclasts crawl along the bone surfaces digging pits as they break down bone surfaces .
Bone Remodeling • Bone is dynamic and active tissue • Long bone growth is accompanied by almost continuous remodeling in order to maintain proper proportions • Large amounts of bone matrix and thousands of osteocytes are being continually removed and replaced • The small scale architecture of bones changes constantly .
Modeling and Remodeling of Bone • The cellular mechanisms responsible for the adaptation of bone are modeling (construction) and remodeling (reconstruction).II. . • Bone modeling produces a change in the size and shape of bone when new bone is deposited without previous bone resorption. resorption by osteoclasts precedes bone formation by osteoblasts. • Bone remodeling.
Bone Remodeling • The spongy bone of the skeleton is replaced every 3 years • The compact bone is replaced every 10 years • The remodeling process is not uniform as some parts experiencing more stress are replaced at a faster rate (every 5-6 months) while other areas change more slowly .
Bone as a load sensing tissue • Bone tissue architecture is influenced by mechanical stresses. . This idea was first • documented by Galilei in 1638 (Galilei 1638) when he suggested that the shape of • bones is related to loading.
• to the lack of them. 2006). . (Frost 1987). In principle. this means that bone is • deposited in sites subjected to stress and is resorbed from sites where there is little • stress (Robling et al. and on the other hand. Bone develops or adapts its structure to that most suited to • resist the forces acting upon it (Wolff 1892).(Wolff 1892). • the • remodeling of bone occurs in response to physical stresses.
.Frost’s mechanostat theory.
Frost‟s mechanostat • Disuse: Strain < circa 800μStrain: Remodeling (bone adaptation and bone repair) Bone mass and bone strength is reduced. • • • . 1500μStrain: Remodeling (bone repair) Bone mass and bone strength stays constant Overload: Strain > circa 1500μStrain: Modeling (bone growth) bone mass and bone strength his increased Fracture: Strain > circa 15000μStrain: maximum elastically deformation excceded . Adapted State: strain between ca.bone fracture. 800μStrain and ca.
• Mechanical stimuli elicit the proliferation of bone • cells .• a stress diversion design. which promotes bone growth and maturation under normal loading conditions.
DNAis stained with DAPI (blue). (Aand B) Primary cilia stained with anti-acetylated-tubulin (red) extend from centrosomes stained with anti-CEP135 (green) in MC3T3-E1 osteoblasts (A) and MLO-Y4 osteocytes (B).• • • • • • • • • • • Primary cilia project from the apical surface of bone cells and bend during fluid flow. DNA is stained with DAPI (blue). (D) Side view of a primary cilium (arrowheads) extending from the apical surface of an MC3T3-E1 osteoblast before (Upper) and during (Lower) application fluidflowfrom left to right. (Scale bars: 5 m. (C) Maximum projection of a confocal z series shows a primary cilium marked by acetylated -tubulin (red) extending from the apical surface marked by CMFDA (green) of an MC3T3-E1 osteoblast. Images are inverted frames from SI Movie 1.) .
Western blot for actin is a loading control. . DNA is stained with DAPI (blue). (C) Polaris siRNA-treated MC3T3-E1 osteoblast showing reduced polaris staining (green) and the absence of a primary cilium extending from the centrioles (arrowhead).• • • • • • • • • • 2. Stable cytoplasmic microtubules are marked by acetylated -tubulin (red) and DNA is stained with DAPI (blue). (Scale bars: 10 m. (B) Control MC3T3-E1 osteoblast showing polaris (green) at the primary cilium (arrowhead) marked by acetylated -tubulin (red). RNAi of polaris prevents primary cilium formation in cultured bone cells. (A) Western blot showing reduced levels of protein in MC3T3-E1 osteoblasts transfected with polaris siRNA (right lane) relative to cells transfected with control siRNA (left lane).
.PRNCIPLES OF DENTAL IMPLANT DESIGN A) Gain initial stability that would reduce the threshold for the „tolerated micromotion‟ and minimize the waiting-period required for loading the implant. C) Design features that maystimulate bone formation. and/ or facilitate bone healing (secondary osseointegration).that would diminish the effect of shear forces on the interface (such as surface roughness related and thread features) so that marginal bone is preserved). B) Incorporate design factors.
Factors concerning implant design which affect the stress distribution to the periimplant bone of loaded dental implants. .
BASIC THREAD TERMINOLOGY .
Illustrates 1.BONE REMODELING SUBSEQUENT TO ABUTMENT CONNECTION .5 to 2 mm of crestal bone loss from implant-abutment interface. . Figure 1.5 to 2 mm of crestal bone loss from implant-abutment interface. Illustrates 1.
. the first bone-to-implant contact was located 1.5 to 2 mm apical to the microgap between the 2 pieces (Figure 1).• 1) The rough/smooth border on 1-piece nonsubmerged implants determines the initial bone-to-implant contact. • (2) In 2-piece implants.7 • (3) Osseous changes occur after the creation of a microgap at the implant-abutment interface.
Horizontal component of bone loss after abutment connection .Pattern of bone loss Horizontal component of bone loss after abutment connection Figure 2.
07 mm) .CONSEQUENCES OF CRESTAL BONE CHANGES epithelial attachment (0.097 mm) Figure 3. The components of biologic connective tissue attachment (1.
9 Histologically. • keratinized oral epithelium and nonkeratinized junctional epithelium. • a pseudo-attachment via hemidesmosomes exists around endosseous implants • connective tissue fibers mechanically insert into root cementum • a tight cuff is formed around titanium implants. • differences • the attachment of the junctional epithelium to teeth is mediated by glycoproteins. .The dentogingival and peri-implant complexes • similar in their cellular composition.
• for an implant-implant relationship the mean papilla length was 4. • Adequate interdental soft tissue depends on the height of the interproximal bone and its relation to the contact point • When the distance from the contact point to the interproximal height of bone is greater than 5 mm.5 mm.• The interproximal height of bone (IHB) has a distinct influence on interdental papillae • mean papilla length for an implant-tooth relationship was found to be 6. avoiding the “black triangle” is difficult .5 mm.
.Implant proximity limitations are obeyed. Maintenance of IHB.
resulting in loss of IHB.Figure 4. Figure 5. . Infringement of pr Infringement of proximity limitations. Implant proximity limitations are obeyed. Maintenance of IHB.
• .5 mm).• If proximity guidelines were not obeyed when placing the implant next to an adjacent implant (3 mm) or tooth (1. then interproximal bone will be insufficient to support papilla formation (and a “black triangle” may be evident.
CONTROLLING CRESTAL BONE LOSS Figure 7.” . platform switching.
“platform switching.” . using a smaller abutment.• Use of nonsubmerged implants to eliminate bone loss is a proven way to accomplish this • A scalloped implant platform has been developed to follow the osseous architecture and eliminate crestal bone loss by maintaining the microgap in a supracrestal position • medializing the position of the microgap. ie.
Radiograph illustrating medialization of microgap. maintenance of crestal bone. .
.minimal remodeling of the interproximal bone and the absence of bone loss relative to restorative platforms.
three days after implant placement.Radiograph at abutment connection. . The implant restorative platforms of the abutments and implants are subcrestal.
maintenance of IHB. .2 medialization of microgap.
platform switching in posterior maxilla. Note maintenance of bone .
Note maintenance of softtissue contours.Implant restoration of central incisor. .