Cryopreserved, Thin, Laser-Etched Osteochondral Allograft Maintains the Functional Components of Articular Cartilage After Two Years of Storage

Abstract Background : Despite improvements in treatment options and techniques, articular cartilage repair continues to be a challenge for orthopedic surgeons. This study provides data to support that the 2-year Cryopreserved, Thin, Laser-Etched Osteochondral Allograft (T-LE Allograft) embodies the necessary viable cells, protein signaling, and extracellular matrix (ECM) scaffold found in fresh cartilage in order to facilitate a positive clinical outcome for cartilage defect replacement and repair. Methods: Viability testing was performed by digestion of the graft, cells were counted using a trypan blue assay. Growth factor and ECM protein content was quantified using biochemical assays. A fixation model was introduced to assess tissue outgrowth capability and cellular metabolic activity in vitro . Histological and immunofluorescence staining were employed to confirm tissue architecture, cellular outgrowth, and presence of ECM. The effects of the T-LE Allograft to signal bone marrow-derived mesenchymal stem cell (BM-MSC) migration and chondrogenic differentiation were evaluated using in vitro co-culture assays. Immunogenicity testing was completed using flow cytometry analysis of cells obtained from digested T-LE Allografts and fresh articular cartilage. Results: Average viability of the T-LE Allograft post-thaw was found to be 94.97 ±3.38%, compared to 98.83 ±0.43% for fresh articular cartilage. Explant studies from the in vitro fixation model confirmed the long-term viability and proliferative capacity of these chondrocytes. Growth factor and ECM proteins were quantified for the T-LE Allograft revealing similar profiles to fresh articular cartilage. Cellular signaling of the T-LE Allograft and fresh articular cartilage both exhibited similar outcomes in co-culture for migration and differentiation of BM-MSCs. Flow cytometry testing confirmed the T-LE Allograft is immune-privileged as it is negative for immunogenic markers and positive for chondrogenic markers. Conclusions: Using our novel, proprietary cryopreservation method, the T-LE Allograft retains excellent cellular viability, with native-like growth factor and ECM composition of healthy cartilage after two years of storage at -80 o C. The successful cryopreservation of the T-LE Allograft alleviates the limited availably of conventionally used fresh osteochondral allograft (OCA), by providing a readily available and simple to use allograft solution. The results presented in this paper supports clinical data that the T-LE Allograft can be a successful option for repairing chondral defects.

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Cryopreserved, Thin, Laser-Etched Osteochondral Allograft Maintains the Functional Components of Articular Cartilage After Two Years of Storage

10.21203/rs.3.rs-34944/v1 ◽

2020 ◽

Author(s):

Carolyn B Rorick ◽

Jordyn A Mitchell ◽

Ruth H Bledsoe ◽

Michael L Floren ◽

Ross M Wilkins

Keyword(s):

Flow Cytometry ◽

Articular Cartilage ◽

Growth Factor ◽

Treatment Options ◽

Osteochondral Allograft ◽

Protein Signaling ◽

Chondral Defects ◽

Healthy Cartilage ◽

Functional Components

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Cryopreserved, Thin, Laser-Etched Osteochondral Allograft maintains the functional components of articular cartilage after 2 years of storage

Journal of Orthopaedic Surgery and Research ◽

10.1186/s13018-020-02049-y ◽

2020 ◽

Vol 15 (1) ◽

Author(s):

Carolyn B. Rorick ◽

Jordyn A. Mitchell ◽

Ruth H. Bledsoe ◽

Michael L. Floren ◽

Ross M. Wilkins

Keyword(s):

Flow Cytometry ◽

Articular Cartilage ◽

Growth Factor ◽

Treatment Options ◽

Osteochondral Allograft ◽

Protein Signaling ◽

Chondral Defects ◽

Healthy Cartilage ◽

Functional Components

Abstract Background Despite improvements in treatment options and techniques, articular cartilage repair continues to be a challenge for orthopedic surgeons. This study provides data to support that the 2-year Cryopreserved, Thin, Laser-Etched Osteochondral Allograft (T-LE Allograft) embodies the necessary viable cells, protein signaling, and extracellular matrix (ECM) scaffold found in fresh cartilage in order to facilitate a positive clinical outcome for cartilage defect replacement and repair. Methods Viability testing was performed by digestion of the graft, and cells were counted using a trypan blue assay. Growth factor and ECM protein content was quantified using biochemical assays. A fixation model was introduced to assess tissue outgrowth capability and cellular metabolic activity in vitro. Histological and immunofluorescence staining were employed to confirm tissue architecture, cellular outgrowth, and presence of ECM. The effects of the T-LE Allograft to signal bone marrow-derived mesenchymal stem cell (BM-MSC) migration and chondrogenic differentiation were evaluated using in vitro co-culture assays. Immunogenicity testing was completed using flow cytometry analysis of cells obtained from digested T-LE Allografts and fresh articular cartilage. Results Average viability of the T-LE Allograft post-thaw was found to be 94.97 ± 3.38%, compared to 98.83 ± 0.43% for fresh articular cartilage. Explant studies from the in vitro fixation model confirmed the long-term viability and proliferative capacity of these chondrocytes. Growth factor and ECM proteins were quantified for the T-LE Allograft revealing similar profiles to fresh articular cartilage. Cellular signaling of the T-LE Allograft and fresh articular cartilage both exhibited similar outcomes in co-culture for migration and differentiation of BM-MSCs. Flow cytometry testing confirmed the T-LE Allograft is immune-privileged as it is negative for immunogenic markers and positive for chondrogenic markers. Conclusions Using our novel, proprietary cryopreservation method, the T-LE Allograft, retains excellent cellular viability, with native-like growth factor and ECM composition of healthy cartilage after 2 years of storage at − 80 °C. The successful cryopreservation of the T-LE Allograft alleviates the limited availably of conventionally used fresh osteochondral allograft (OCA), by providing a readily available and simple to use allograft solution. The results presented in this paper supports clinical data that the T-LE Allograft can be a successful option for repairing chondral defects.

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Combined Effects of Bone Marrow-Derived Mesenchymal Stem Cells and PLGA-PEG-PLGA Scaffolds on Repair of Articular Cartilage Defect

Advanced Materials Research ◽

10.4028/www.scientific.net/amr.815.345 ◽

2013 ◽

Vol 815 ◽

pp. 345-349 ◽

Cited By ~ 2

Author(s):

Ching Wen Hsu ◽

Ping Liu ◽

Song Song Zhu ◽

Feng Deng ◽

Bi Zhang

Keyword(s):

Stem Cells ◽

Mesenchymal Stem Cells ◽

Articular Cartilage ◽

Growth Factor ◽

Cartilage Defect ◽

Cartilage Regeneration ◽

Tissue Growth ◽

Cartilage Defects

Here we reported a combined technique for articular cartilage repair, consisting of bone arrow mesenchymal stem cells (BMMSCs) and poly (dl-lactide-co-glycolide-b-ethylene glycol-b-dl-lactide-co-glycolide) (PLGA-PEG-PLGA) triblock copolymers carried with tissue growth factor (TGF-belat1). In the present study, BMMSCs seeded on PLGA-PEG-PLGA with were incubated in vitro, carried or not TGF-belta1, Then the effects of the composite on repair of cartilage defect were evaluated in rabbit knee joints in vivo. Full-thickness cartilage defects (diameter: 5 mm; depth: 3 mm) in the patellar groove were either left empty (n=18), implanted with BMMSCs/PLGA (n=18), TGF-belta1 modified BMMSCs/PLGA-PEG-PLGA. The defect area was examined grossly, histologically at 6, 24 weeks postoperatively. After implantation, the BMMSCs /PLGA-PEG-PLGA with TGF-belta1 group showed successful hyaline-like cartilage regeneration similar to normal cartilage, which was superior to the other groups using gross examination, qualitative and quantitative histology. These findings suggested that a combination of BMMSCs/PLGA-PEG-PLGA carried with tissue growth factor (TGF-belat1) may be an alternative treatment for large osteochondral defects in high loading sites.

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The Molecular Pathogenesis of Haemangioma

10.26686/wgtn.16945627 ◽

2021 ◽

Author(s):

◽

Anasuya Vishvanath

Keyword(s):

Growth Factor ◽

Tyrosine Kinases ◽

Molecular Mechanisms ◽

Therapeutic Potential ◽

Primary Tumour ◽

Treatment Options ◽

Janus Kinase ◽

Stem Cell Population ◽

Induced Apoptosis

<p>Haemangioma is a primary tumour of the microvasculature characterised by active angiogenesis and endothelial cell (EC) proliferation followed by slow regression or involution whereby the newly formed blood vessels are gradually replaced by fibrofatty tissue. These developmental changes have been arbitrarily divided into the proliferative, involuting and involuted phases. The cellular and molecular events that initiate and regulate the proliferation and spontaneous involution of haemangioma remain poorly understood. This study examined the expression of a number of genes known to be associated with angiogenesis. These include members of the signal transducers and activators of transcription (STAT) protein family of transcription factors, STAT-3 and STAT-1, and the endothelial receptor tyrosine kinases, VEGFR-1 and VEGFR-2. While STAT-3, STAT-1 and VEGFR-1 expression was detected in all phases of haemangioma, VEGFR-2 expression was found to be abundant only during the proliferative phase and decreased with ongoing involution. In this study the cellular structures that form capillary-like outgrowths in an in vitro haemangioma explant model were characterised as haemangioma-derived mesenchymal stem cells (HaemDMSCs) while the cells obtained directly from dissociated proliferative haemangioma tissue were defined as haemangioma-derived endothelial progenitor cells (HaemDEPCs). This investigation showed that although the vascular endothelial growth factor (VEGF), a key growth factor for ECs, was able to maintain HaemDEPCs morphology and immunophenotype for a limited period, these cells eventually differentiated into HaemDMSCs, which subsequently differentiated into adipocytes. Furthermore, while VEGF induced significant capillary-like sprouting from tissue explants, both capillary-like sprouting and HaemDMSCs proliferation was inhibited by the addition of AG490, a Janus kinase (JAK) inhibitor which has also been shown to inhibit the STAT protein pathway. These findings indicate that the development and differentiation of a progenitor cell and a stem cell population underlies the aethiopathogenesis of haemangioma and that VEGF and STAT signalling is involved in the programmed life-cycle of haemangioma. The in vitro explant model for haemangioma offers an opportunity to study and identify novel treatment options for haemangioma. Interferon-alpha (IFN ) has been used to treat steroid-resistant haemangioma but is associated with serious side-affects. The tumour necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) has been shown to specifically induce apoptosis of cancer cells while sparing normal cells. As IFN has previously been shown to sensitise cells to TRAIL-induced apoptosis, this study examined the efficacy of low dose IFN in combination with TRAIL in the in vitro explant model and also in the purified HaemDMSCs. Results showed that combining IFN with TRAIL led to synergistic inhibition of capillary-like outgrowth. These results indicate that IFN in combination with TRAIL serves as a potential treatment option for haemangioma. In contrast, HaemDMSCs were protected from TRAIL-induced killing. These cells were found to express high levels of the decoy receptors, osteoprotegerin (OPG) and decoy receptor 2 (DcR2). Increased OPG expression was also detected in the extracellular matrix and in the conditioned medium of HaemDMSCs. From these findings, we postulate that the increased level of extracellular OPG by HaemDMSCs is a stress response induced by their in vitro expansion and that secreted OPG functions as a protective shield preventing TRAIL action. The empirical and unsatisfactory nature of the current therapies for haemangioma underscores the importance of a scientific approach to this common tumour. A better understanding of the molecular mechanisms that govern haemangioma is of both clinical and biological interest as it may provide vital information with therapeutic potential for haemangioma and also for other angiogenesis-dependent conditions.</p>

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Evaluation of Morphine with Imiquimod as Opioid Growth Factor Receptor or Nalmefene as Opioid Blocking Drug on Leishmaniasis Caused by Leishmania major in Vitro

Iranian Journal of Parasitology ◽

10.18502/ijpa.v14i3.1478 ◽

2019 ◽

Cited By ~ 1

Author(s):

Javad JABARI ◽

Fatemeh GHAFFARIFAR ◽

John HORTON ◽

Abdolhosein DALIMI ◽

Zohreh SHARIFI

Keyword(s):

Flow Cytometry ◽

Growth Factor ◽

Leishmania Major ◽

Growth Factor Receptor ◽

Adjunctive Treatment ◽

Control Group ◽

High Dose ◽

Macrophage Infection ◽

Opioid Growth Factor

Background: In this research, the effect of morphine on promastigotes and amastigotes of Leishmania major has been investigated in the presence of nalmefene as a blocking opioid drug and imiquimod as an opioid growth factor receptor. Methods: This study was conducted at Tarbiat Modares University, Tehran, Iran in 2015-2018. Morphine with different concentration (0.1, 1, 10 and 100 1µg/ml) alone and with imiquimod (0.01, 0.1 and 1µg/ml) and nalmefene (0.1, 1 and 10 µg/ml) on promastigotes and amastigotes in macrophages and also the percentage of infected macrophages was investigated. For evaluation of the apoptosis, we used flow cytometry method. The effect of imiquimod and nalmefene on glucantime and amphotericin B as current drugs for treatment of leishmaniasis was evaluated too. Results: The effect of morphine on promastigotes and amastigotes has a reverse relationship with its concentration. The results of flow cytometry for drug-treated promastigotes revealed that apoptosis and necrosis did not increase markedly relative to the control group. A combination of morphine and imiquimod in concentrations of 0.05, 5 and 5 µg/ml had a pronounced effect on reduction and prevention of macrophage infection with amastigotes. Morphine at a concentration of 0.1 µg/ml plays the role of adjunctive treatment. In amastigote assay we found the better results in group that get glucantime 25 µg/ml+ imiquimod 0.5 µg/ml. Conclusion: This effect is strengthened with imiquimod and weakened with nalmefene. Using high dose morphine and nalmefene had reverse effects. They suppress immune system and had no controlling effect in macrophages amastigote infection and reduction of promastigotes.

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Increased Marrow CD57+ Cytotoxic T Cells Is a Powerful Prognostic Marker for Survival in Patients with Relapsed Multiple Myeloma (MM) Receiving Thalidomide.

Blood ◽

10.1182/blood.v106.11.3486.3486 ◽

2005 ◽

Vol 106 (11) ◽

pp. 3486-3486

Author(s):

Linda R. Mileshkin ◽

Peter Gambell ◽

Victoria Beshay ◽

Yoshihiro Hayakawa ◽

Mark Smyth ◽

...

Keyword(s):

Flow Cytometry ◽

T Cells ◽

Growth Factor ◽

Cytotoxic T Cells ◽

Univariate Analysis ◽

Median Number ◽

T Cell Subsets ◽

Phase 2 Trial ◽

Baseline Levels

Abstract Background: In vitro studies indicate that thalidomide alters the marrow microenvironment and also has an immunoregulatory role. We assessed various laboratory and clinical parameters to examine potential prognostic markers and to assess for changes during thalidomide therapy. Methods: 75 patients with relapsed/refractory MM were enrolled in a multi-centre phase 2 trial using thalidomide (Blood. 2003;102:69–77). Platelet-poor plasma (PPP) and marrow biopsy were obtained at baseline and 3 monthly and immunohistochemistry for CD34, VWF, mast cell tryptase and CD57 performed. Flow cytometry on marrow aspirates was used to define the CD57+ population (T cell subsets, NK, NKT markers used). Vascular endothelial growth factor (VEGF), basic-Fibroblast growth factor (bFGF), interleukin-6 (IL-6) and Hepatocyte growth factor (HGF) were measured in PPP. Objectives were to examine for effect on response rate (RR), progression-free (PFS) and overall survival (OS). Results: Overall RR was 28% with 55% stable disease. Only VEGF predicted response-no responses seen in patients with a level of 0, compared to a RR of 34% in those with VEGF > 0 (p=0.015). Microvessel density (MVD) did not predict for response, PFS or OS. The median number of CD57+ cells at baseline was 3 per HPF (range: 0–27) and flow cytometry confirmed that CD57+ cells were predominantly cytotoxic T cells. CD57+ cells did not predict for response, however on univariate analysis elevated levels were the major predictor of better OS (p=0.003). Predictors for inferior OS were raised baseline levels of IL-6 (p=0.014), and HGF (p=0.016). Multivariate analysis for OS which incorporated clinical variables demonstrated age >65 yrs (p=0.009), raised LDH (p=0.008) and zero baseline CD57+ cells (p=0.011) as predictors of inferior OS. MVD and VEGF fell significantly in responding patients although CD57+ cells did not change. Conclusion: Levels of VEGF and MVD decline in thalidomide responders. However, high baseline angiogenic activity was not necessary to obtain a response. Increased age and elevated LDH are important predictors of poorer OS, with elevated baseline levels of CD57+ cells being an independent predictor of superior outcome.

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Perturbed Endocytosis as a Mechanism of CALM-Dependent Leukemogenesis: Identification of Specific CALM Domains Required for Internalization and Demonstration of Prolonged JAK2 Signaling in Response to GM-CSF.

Blood ◽

10.1182/blood.v110.11.1817.1817 ◽

2007 ◽

Vol 110 (11) ◽

pp. 1817-1817

Author(s):

Natasha L. Brooks ◽

David A. Erichsen ◽

Daniel S. Wechsler

Keyword(s):

Flow Cytometry ◽

Growth Factor ◽

Cell Lines ◽

Fusion Proteins ◽

Geometric Mean ◽

Leukemia Cell ◽

Growth Factor Signaling ◽

Gm Csf ◽

Leukemia Cell Lines

Abstract Background: Clathrin Assembly Lymphoid Myeloid leukemia (CALM) gene rearrangements, in which CALM is fused to MLL or AF10 genes, are found in aggressive leukemias and lymphomas. Expression of MLL-CALM or CALM-AF10 fusion proteins immortalizes murine hematopoietic cells in vitro, correlating with leukemogenesis in vivo. While disrupted MLL or AF10 activity contributes to transformation, perturbation of normal CALM function may also play a role. The native CALM protein is primarily cytoplasmic and functions in Clathrin-Dependent Endocytosis (CDE). We have previously shown that overexpression of CALM-containing fusion proteins in COS7 cells impairs CDE of both Transferrin (TF) and Epidermal Growth Factor (EGF). These initial observations were made using a qualitative (but time-consuming) visual assay of Texas Red (TR)-labeled TF or EGF. We confirmed these results using a semi-quantitative radioactive assay (with 131I-TF or EGF) that, while sensitive, lacked specificity for transfected cells. Here we describe the development of a flow cytometry-based assay of CDE that permits specific quantitation in cells transfected with CALM-containing proteins. We also measure downstream effects of perturbed CDE on growth factor signaling. Objectives: To validate a novel flow cytometry-based CDE assay; To identify CALM domains that play critical roles in CDE; To analyze kinetics of phosphorylation of JAK2, a downstream target of growth factor signaling, during perturbed CDE. Methods: COS7 cells transfected with GFP-tagged CALM-containing constructs were incubated at 4°C for 1h with AlexaFluor (AF) 633-TF or AF647-EGF to allow binding, followed by incubation at 25°C (5, 10, or 15 min) to permit internalization. Following acid buffer wash and fixing (1% formalin/PBS), internalized fluorescence was measured by flow cytometry. Geometric mean fluorescence intensities of GFP+/AF+ populations were normalized to respective 4°C controls. JAK2 phosphorylation was assessed by western blotting at various time intervals following GM-CSF stimulation of six different leukemia cell lines. Results: Overexpression of CALM-containing constructs in COS7 cells resulted in a reduced rate of TF or EGF internalization. Native CALM (N-CALM1–660) overexpression reduced the rate of TF and EGF internalization by 53%. The portion of CALM found in MLL-CALM fusions, CALM256–660, reduced TF and EGF internalization by 66% compared with controls. CALM436–583 overexpression reduced the rate of TF and EGF internalization by 43%. A series of CALM deletion constructs (CALM256–492, CALM256–502, CALM337–531, CALM593–660, and CALM601–660) did not perturb internalization of TF or EGF. Thus, the presence of a 52 amino acid (aa) region from CALM aa 531–583 was required to perturb internalization. Phosphorylation of JAK2 was prolonged in the setting of CALM-AF10 expression (U937 and P31/Fuji cells) compared with cell lines that do not express CALM-AF10 (HL60, K562, MonoMac6, THP1), likely as a consequence of perturbed CDE. Conclusions: We demonstrate that CALM-dependent perturbation of CDE in COS7 cells can be measured by a novel flow cytometry-based approach. Use of this rapid, quantitative assay narrows the specific region of CALM critical to CDE perturbation to 52 aa. We also show that signaling downstream of growth factors is enhanced during perturbed CDE in leukemia cell lines. These observations support an underappreciated role for CDE dysregulation in leukemogenic transformation.

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Protection from interleukin 1 induced destruction of articular cartilage by transforming growth factor beta: studies in anatomically intact cartilage in vitro and in vivo.

Annals of the Rheumatic Diseases ◽

10.1136/ard.52.3.185 ◽

1993 ◽

Vol 52 (3) ◽

pp. 185-191 ◽

Cited By ~ 77

Author(s):

H M van Beuningen ◽

P M van der Kraan ◽

O J Arntz ◽

W B van den Berg

Keyword(s):

Articular Cartilage ◽

Growth Factor ◽

Transforming Growth Factor Beta ◽

Transforming Growth Factor ◽

Interleukin 1 ◽

Intact Cartilage ◽

Growth Factor Beta

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Altered swelling and ion fluxes in articular cartilage as a biomarker in osteoarthritis and joint immobilization: a computational analysis

Journal of The Royal Society Interface ◽

10.1098/rsif.2014.1090 ◽

2015 ◽

Vol 12 (102) ◽

pp. 20141090 ◽

Cited By ~ 12

Author(s):

Sara Manzano ◽

Raquel Manzano ◽

Manuel Doblaré ◽

Mohamed Hamdy Doweidar

Keyword(s):

Articular Cartilage ◽

Computational Model ◽

Three Dimensional ◽

Ion Distribution ◽

Tissue Degeneration ◽

Structural Deterioration ◽

Healthy Cartilage ◽

Tissue Degradation

In healthy cartilage, mechano-electrochemical phenomena act together to maintain tissue homeostasis. Osteoarthritis (OA) and degenerative diseases disrupt this biological equilibrium by causing structural deterioration and subsequent dysfunction of the tissue. Swelling and ion flux alteration as well as abnormal ion distribution are proposed as primary indicators of tissue degradation. In this paper, we present an extension of a previous three-dimensional computational model of the cartilage behaviour developed by the authors to simulate the contribution of the main tissue components in its behaviour. The model considers the mechano-electrochemical events as concurrent phenomena in a three-dimensional environment. This model has been extended here to include the effect of repulsion of negative charges attached to proteoglycans. Moreover, we have studied the fluctuation of these charges owning to proteoglycan variations in healthy and pathological articular cartilage. In this sense, standard patterns of healthy and degraded tissue behaviour can be obtained which could be a helpful diagnostic tool. By introducing measured properties of unhealthy cartilage into the computational model, the severity of tissue degeneration can be predicted avoiding complex tissue extraction and subsequent in vitro analysis. In this work, the model has been applied to monitor and analyse cartilage behaviour at different stages of OA and in both short (four, six and eight weeks) and long-term (11 weeks) fully immobilized joints. Simulation results showed marked differences in the corresponding swelling phenomena, in outgoing cation fluxes and in cation distributions. Furthermore, long-term immobilized patients display similar swelling as well as fluxes and distribution of cations to patients in the early stages of OA, thus, preventive treatments are highly recommended to avoid tissue deterioration.

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Treatment of Unicompartmental Cartilage Defects of the Knee with Unicompartmental Knee Arthroplasty, Patellofemoral Partial Knee Arthroplasty or Focal Resurfacing

Life ◽

10.3390/life11050394 ◽

2021 ◽

Vol 11 (5) ◽

pp. 394

Author(s):

Bernhard Springer ◽

Friedrich Boettner

Keyword(s):

Articular Cartilage ◽

Conservative Treatment ◽

Knee Replacement ◽

Knee Arthroplasty ◽

Treatment Options ◽

Cartilage Defects ◽

Osteoarthritis Of The Knee ◽

Chondral Defects ◽

Focal Resurfacing ◽

Partial Knee Replacement

Focal chondral defects are common lesions of the articular cartilage. They are predominantly found on the medial femoral condyle and often progress to osteoarthritis of the knee. Various conservative treatment options are available. The conservative treatment might reduce pain and delay the progress of degenerative processes. However, restoration of the articular cartilage cannot be accomplished. If the conservative treatment fails unicompartmental arthroplasty, patellofemoral joint replacement or focal resurfacing are reasonable options to postpone total knee arthroplasty. A careful patient selection before surgery is crucial for all three treatment options. The following overview reports indications and outcomes of medial partial knee replacement, patellofemoral partial knee replacement, and focal resurfacing treatment options for focal chondral defects.

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