bone remodeling rate

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.

phases of bone remodelling

: activation, resorption, reversal, 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).

 Concurrently with osseointegration process, bone remodelling occurs, where the bone density is changed due to the implant induced mechanical loading [5]. Therefore, bone remodelling is in essence a process where the bone changes its own property to adapt to its changing mechanical loading environment [6]. As bone remodels positively, the quality of the bone will improve, therefore leading to the stabilization of the dental implant inside the dental bone. This will have the effect of reducing the rate of implant failure. Therefore, in order to optimize the dental implant design, it is crucial to understand the magnitude and the development of mechanical stress inside the bony tissues. Such predictions can help to minimize the possibility of implantation failure.

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

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 (-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.

Lrp5 appears to be a potent regulator of bone mass, size, and strength. One of the main mechanisms of action for the receptor in bone is through mechanical signaling, Lrp5 is a late-acting mediator in the osteogenic response to mechanical loading, suggesting that skeletal fragility in individuals afflicted with OPPG might be related to inadequate processing of signals derived from mechanical stimulation.

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, respectively. Internally-generated tension and forces transmitted through cell-cell contact similarly reach focal adhesions through the cytoskeleton. Forces concentrated within the focal adhesion (magnified at bottom of figure) can stimulate integrin clustering and induce recruitment of additional cytoskeletal linker proteins (Vin, vinculin; Pax, paxillin; Tal, talin) that connect directly to microfilaments and indirectly to microtubules. Forces applied to this specialized cytoskeletal adhesion complex also activate integrin-associated signal cascades. Focal adhesion kinase (FAK) may be involved in Shc recruitment as well as modulation of Rho activity which, in turn, can regulate the force response through mDia1. Caveolin-1 (cav-1) can also recruit Shc to integrins to activate the ERK cascade. CD47 associates with the integrin heterodimer to form a protein complex with seven transmembrane segments that mimics the action of G protein-coupled receptors. In the case shown, when integrins are mechanically stressed, the complex stimulates Gs-mediated up-regulation of the cAMP cascade through adenylate cyclase (AC), resulting in nuclear translocation of the catalytic subunit of protein kinase A, PKA-c

Factors affecting bone modling and remodling around dental implant

In non-human primate studies, it was observed that five out of eight implants lost osseointegration due to excessive occlusal overloading after 4.515.5 months of loading (Isidor 1996, 1997). Among the three remaining implants, one showed severe crestal bone loss and the other two showed the highest bone implant contact and density. The results suggested that implant loading might have significantly affected the responses of periimplant osseous structures. However, it should be noted that the loss of osseointegration observed might have been attributed to the unrealistically high-occlusal overload used in the study

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). Low-magnitude high frequency (30-50 Hz) mechanical signals produce, instead, anabolic effects on bone. If such loading regimens could be applied for dental implants, a favorable mechanical environment for osseointegration is promoted. Bone-implant interface maturation could be faster because bone deposition increases.

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

Preserving the Bone Level Marginal bone remodeling is obviously a multifactorial issue. The surgery-induced trauma can be highly detrimental for the release of a flap and induces some cell death, which provokes an inflammatory process and brings mediators of bone resorption. The more the bone is exposed and dried by suction, the more bone resorption occurs. This is the rationale for the use of conservative surgical approaches in these procedures.

 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

 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, 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

 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

 Bone Morphogenetic Proteins These are included in the TGF- family

Except BMP-1

BMP2-7,9 are osteoinductive BMP2,6, & 9 may be the most potent in osteoblastic differentiation Work through the intracellular Smad pathway Follow a dose/response ratio

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

Importance of mechanical aspects

If we know the mechanical aspect well, then one can control bone remodeling through mechanical stress that applied through exercise either voluntarily or with the help of mechanical devices. (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

 Platelet-Derived Growth Factor

A dimer of the products of two genes, 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

 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

 Cytokines
Interleukin-1,-4,-6,-11, 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

Specific Factor Stimulation of Osteoblasts and Osteoclasts

Osteoclasts
Cytokine Resorption IL-1 TNF- TNF- TGF- TGF- 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

species
Table 1. Summary of four key attributes in terms of similarity between animal and human bone.

Canine
Macrostructure Microstructure Bone Composition Bone Remodelling ++ ++ +++ ++

Sheep/Goat Pig
+++ + ++ ++ ++ ++ +++ +++

Rabbit
+ + ++ +

+ least similar, ++ moderately similar, +++ most similar.

Signficans of bone remodling

responsible for removal and repair of damaged bone to maintain integrity of the adult skeleton and mineral homeostasis.

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.htm

. Currently available bone biochemical markers.

. A. 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. 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

BMU Remodeling Sequence

www.ifcc.org/ejifcc/ vol13no4/130401004n.htm

Osteocytes

Activation Quiescence Resorption

Formation & Mineralization

Reversal

 Endocrine
STH (somatotropic or growth hormone): increases cell division & all subsidiary processes (total protein synthesis, net protein synthesis, total turnover, tissue growth) ACH (adrenal-cortical hormone) : decreases cell division & subsidiary processes. T4 (thyroxine): affects all tissues. Estrogens: selectively decrease cell division & subsidiary processes; affect cartilage & lamellar bone. Vitamins A, C & D & calcitonin

12.6.2 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. Biochemical activity of calcium Straining bone increases calcium concentration in interstitial fluid Change in solubility of HA crystals in response to stress

Stress-controlled bone development

Compressive stress stimulates formation of new bone and important factor in fracture healing During immobilization, net loss of bone calcium & phosphorous; after resume of normal activity mineral loss phenomena reversed ! Astronauts subjected to weightlessness has same results: subnormal stresses causes loss of bone strength, radiographic opacity & size. 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. Rigid plate fixation in dog yields thinning of femoral diaphysis cortex rather than osteoporosis

Bone Remodeling
Bone of the skeleton are continually remodeled for 2 reasons
Bone remodeling helps maintain constant concentrations of Ca2+ and PO43- 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

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, fluoride, 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, John Wiley & Sons, Inc. 61

medications
Simvastatin is a lipid lowering agent with osteoanabolic effects. Histomorphometric studies have shown increased bone ingrowth and mechanical examination, increased interface strength, superior stability and osseous adaptation at the bone/implant interface in the simvastatintreated group3

Aging and Bone Tissue

The level of sex hormones diminishes during middle age, especially in women after menopause. A decrease in bone mass occurs. Bone resorption by osteoclasts outpaces bone deposition by osteoblasts. Female bones generally are smaller and less massive than males. Loss of bone mass in old age has a greater adverse effect in females.
Copyright 2009, John Wiley & Sons, Inc.

63

 Bisphosphonates inhibit osteoclast-mediated bone resorption and normalize the high rate of bone turnover that characterizes osteoporosis. Consequently, there is a rationale for using bisphosphonates to enhance early stability of implants in patients with low bone mass30,62,89-

 indomethacin causes a transient decrease in attachment strength at early periods, but it does not seem to significantly affect longterm osseointegration of porous-coated implants98.

 warfarin, Enoxaparin, 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.

 fondaparinux, a synthetic anticoagulant substance similar to heparin, showed no inhibitory in vitro effects on human osteoblasts within the concentration range investigated (0.01-100 g/ml). Therefore, fondaparinux may be used to avoid the heparin-related negative influence on osteoblast-dependent fracture healing and endoprosthetic implant integration99,100.

 radiation therapy seems to delay bone remodeling preand post-implantation35,

 Recently, cell-mediated regional gene therapy was introduced to deliver potent morphogens or growth factors in regenerative medicine. 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.

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.

70

 Meloxicam negatively influenced bone healing in the cortical and cancellous bone around titanium implants inserted in rats after continuous administration

Aging and Bone Tissue

Osteoporosis
Condition where bone resorption outpaces bone deposition May be due to depletion of calcium from the body

Copyright 2009, John Wiley & Sons, Inc.

72

Histology of Bone Tissue

Copyright 2009, John Wiley & Sons, Inc.

73

Bone Remodeling
Bone forming osteoblasts form from mesenchyme-like stem cells located in the periosteum, endosteum, 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

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, osteoclasts take up collagen and dead osteocytes by phagocytosis

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

II.Modeling and Remodeling of Bone

The cellular mechanisms responsible for the adaptation of bone are modeling (construction) and remodeling (reconstruction). Bone modeling produces a change in the size and shape of bone when new bone is deposited without previous bone resorption. Bone remodeling, resorption by osteoclasts precedes bone formation by osteoblasts.

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.

(Wolff 1892), (Frost 1987),

the remodeling of bone occurs in response to physical stresses, and on the other hand, to the lack of them. Bone develops or adapts its structure to that most suited to resist the forces acting upon it (Wolff 1892). 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. 2006).

Frosts mechanostat theory.

Frosts mechanostat
Disuse: Strain < circa 800Strain: Remodeling (bone adaptation and bone repair) Bone mass and bone strength is reduced. Adapted State: strain between ca. 800Strain and ca. 1500Strain: Remodeling (bone repair) Bone mass and bone strength stays constant Overload: Strain > circa 1500Strain: Modeling (bone growth) bone mass and bone strength his increased Fracture: Strain > circa 15000Strain: maximum elastically deformation excceded - bone fracture.

 a stress diversion design, which promotes bone growth and maturation under normal loading conditions. Mechanical stimuli elicit the proliferation of bone cells

Primary cilia project from the apical surface of bone cells and bend during fluid flow. (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).DNAis stained with DAPI (blue). (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. 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. Images are inverted frames from SI Movie 1. (Scale bars: 5 m.)

2. 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). Western blot for actin is a loading control. (B) Control MC3T3-E1 osteoblast showing polaris (green) at the primary cilium (arrowhead) marked by acetylated -tubulin (red). 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). Stable cytoplasmic microtubules are marked by acetylated -tubulin (red) and DNA is stained with DAPI (blue). (Scale bars: 10 m.

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. B) Incorporate design factors,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). C) Design features that maystimulate bone formation, and/ or facilitate bone healing (secondary osseointegration).

Factors concerning implant design which affect the stress distribution to the periimplant bone of loaded dental implants.

BASIC THREAD TERMINOLOGY

BONE REMODELING SUBSEQUENT TO ABUTMENT CONNECTION

. Illustrates 1.5 to 2 mm of crestal bone loss from implant-abutment interface.

Figure 1. Illustrates 1.5 to 2 mm of crestal bone loss from implant-abutment interface.

 1) The rough/smooth border on 1-piece nonsubmerged implants determines the initial bone-to-implant contact. (2) In 2-piece implants, the first bone-to-implant contact was located 1.5 to 2 mm apical to the microgap between the 2 pieces (Figure 1).7 (3) Osseous changes occur after the creation of a microgap at the implant-abutment interface.

Pattern of bone loss

Horizontal component of bone loss after abutment connection

Figure 2. Horizontal component of bone loss after abutment connection

CONSEQUENCES OF CRESTAL BONE CHANGES

epithelial attachment (0.097 mm)

Figure 3. The components of biologic

connective tissue attachment (1.07 mm)

The dentogingival and peri-implant complexes

similar in their cellular composition, keratinized oral epithelium and nonkeratinized junctional epithelium.9 Histologically, differences the attachment of the junctional epithelium to teeth is mediated by glycoproteins, 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.

 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 6.5 mm; for an implant-implant relationship the mean papilla length was 4.5 mm. 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, avoiding the black triangle is difficult

Implant proximity limitations are obeyed. Maintenance of IHB.

Figure 4. Implant proximity limitations are obeyed. Maintenance of IHB.

Figure 5. Infringement of pr

Infringement of proximity limitations, resulting in loss of IHB.

 If proximity guidelines were not obeyed when placing the implant next to an adjacent implant (3 mm) or tooth (1.5 mm), 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.

 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, using a smaller abutment. platform switching.

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.

Radiograph at abutment connection, three days after implant placement. The implant restorative platforms of the abutments and implants are subcrestal.

medialization of microgap, maintenance of IHB.

platform switching in posterior maxilla. Note maintenance of bone

Implant restoration of central incisor. Note maintenance of softtissue contours.