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Cartilage Injury and Surgical Treatment PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Cartilage Injury & Surgical Treatment: Microfracture, Cartilage repair/transplant” by Ian Rice MD.

This medical PowerPoint presentation is about cartilage injury and surgical treatment.

Cartilage injuries can be caused by a variety of factors, including sports injuries, aging, and genetic factors. These injuries can lead to pain, stiffness, and reduced mobility, and if left untreated, they can cause permanent damage to the joint.

Surgical treatment for cartilage injuries typically involves one of two approaches: repair or replacement. Repair procedures aim to preserve as much of the patients natural cartilage as possible, while replacement procedures involve replacing damaged cartilage with a synthetic or donor material.

Some common surgical treatments for cartilage injuries include:

Microfracture: This procedure involves creating small fractures in the underlying bone to promote the growth of new cartilage.
Autologous Chondrocyte Implantation (ACI): In this procedure, healthy cartilage cells are harvested from the patient, grown in a laboratory, and then implanted back into the affected joint.
Osteochondral Autograft Transplantation (OATS): This procedure involves transferring healthy cartilage and bone from an unaffected part of the patients joint to the damaged area.
Matrix-Induced Autologous Chondrocyte Implantation (MACI): This procedure involves implanting a scaffold infused with the patients own cartilage cells into the affected area.
Total joint replacement: In severe cases where the joint has sustained extensive damage, a total joint replacement may be necessary. This involves removing the damaged joint and replacing it with an artificial joint.

The choice of surgical treatment depends on the severity and location of the injury, as well as the patients overall health and medical history. Your doctor can help determine which approach is best for you.

Tags : cartilage injury, Microfracture, Autologous Chondrocyte Implantation, Osteochondral Autograft Transplantation, OATS, Matrix-Induced Autologous Chondrocyte Implantation, MACI, Total joint replacement, Orthopaedic Surgery, Orthopaedic Surgery PowerPoint presentation

Published on : Jun 23, 2023 | Views : 1800 | Downloads : 3

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Slide 1-

Cartilage Injury & Surgical Treatment: Microfracture, Cartilage repair/transplant Ian Rice md
Slide 2-

Outline Cartilage Structure Causes of Cartilage Defects Surgical treatments with Level III & IV Evidence Microfracture OAT ACI Comparative Outcomes Level I & II Studies
Slide 3-

Articular Cartilage Decrease friction and distribute load Extracellular matrix Water – 65-80% cartilage mass Larger percentage superficially than deep Decreases with normal aging Increases with arthritis Increased permeability, decreased strength, decreased Young modulus of elasticity
Slide 4-

Articular Cartilage Extracellular matrix Collagen – 10-20% cartilage mass Type II 90-95% Framework and tensile strength Proteoglycans 10-15% of cartilage Compressive strength Attracts water Produced by chondrocytes Composed of GAGs (chondroitin sulfate and keratin sulfate)
Slide 5-

Articular Cartilage Superficial laceration healing: chondrocyte proliferation, but no healing which may be related to avascularity Deep laceration healing (deep to tidemark): fibrocartilage healing Occurs when penetrates into subchondral bone Hematoma  stem cell migration  vascular ingrowth Fibrocartilage produced by undifferentiated marrow mesenchymal stem cells Type I cartilage Decreased resiliency, stiffness, wear characteristics, resistance to arthritis
Slide 6-

Cartilage Lesions Traumatic Injury Osteochondritis Dissecans
Slide 7-

Osteoarthritis Management (AAOS recommendation) NSAIDs (strong) Weight loss (moderate) Exercise/physical therapy (strong) Bracing (equivocal) Corticosteroid injections (inconclusive) Viscoelastic injections (cannot recommend) Arthroscopic debridement (strongly against without mechanical Sx) High tibial osteotomy (limited strength recommendation) Unicompartmental arthroplasty Total joint arthroplasty
Slide 8-

Occult Fractures & Bone Bruises Subchondral and trabecular bone often injured w/ knee trauma Greater recognition using MRI Often encountered with ligamentous injuries - ACL Seen with 70-80% of tears (COR) Found on anterior aspect of lateral femoral condyle, near sulcus terminalis, and on posterior tibial plateau.
Slide 9-

Occult Fractures & Bone Bruises Bone bruises Bleeding and edema from microscopic compression fractures of cancellous bone Thought to result from traumatic impaction between the femoral and tibial condyles Sequelae of bone bruised unclear May lead to subsequent cartilage degeneration
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Occult Fractures & Bone Bruises Evaluation Pts typically present after trauma to knee Joint effusion Key to evaluate for ligamentous injury Imaging Plain films often negative MRI Best on T-2 fat suppressed Short T-1 inversion recovery images
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Occult Fractures & Bone Bruises Treatment Non-op Protected WB until pain/swelling resolve Repair of concomitant injuries as needed Typically return to sports in 3 mos. (COR) Surgical Indications Impaction injury results in > 2mm displacement of articular surface of the weight bearing surface Osteochondral fractures resulting in full focal thickness loss of cartilage Rehab ~6 weeks of NWB Strengthening & ROM exercises begin immediately Return to impact & sport activities in 4-6 months
Slide 12-

Blunt Injuries to Articular Cartilage Treatment Non-op Protected WB until symptoms resolve Unloader bracing with prolonged symptoms Surgical: Indications: Prolonged symptoms or overt damage to the articular surface found on imaging Arthroscopy Chondroplasty: unstable flaps, loose chondral fragments Full thickness chondral defects Discussed later
Slide 13-

Classification of Cartilage Damage
Slide 14-

Classification of Cartilage Damage Paunipagar, et al. (2014) Ind J Rad and Imaging, 24.3: 237-48
Slide 15-

Osteochondritis Dissecans Etiology still remains unclear Repetitive microtrauma Secondary effects of vascular insufficiency Inherited factors Compounded by including traumatic lesions Classification based on location, fragmentation, displacement and status of growth plate Skeletal age at onset of symptoms is most important prognostic factor Influences timing and nature of treatment Incidence: 0.02-0.03% by radiographs, 1.2% by knee arthroscopy Highest rates age 10-15 years Male to female 2:1 Bilateral in 15-30% Crawford, et al. (2006) J Am Acad Orthop Surg 14: 90-100
Slide 16-

Sites of lesions of osteochondritis dissecans of knee according to Heffi et al (A) and Aichroth (B).
Slide 17-

Osteochondritis Dissecans Evaluation Pain w/o history of trauma Typically present with poorly localized pain Exam often yields TTP localized to anteriomedial aspect of knee Persistent swelling/effusion Locking & catching Suggest loose OCD fragments Wilson’s test – pain with internal rotatin of tibia during extension between 90-30deg relieved with external rotation Imaging: AP/lat/sunrise/notch views MRI Size of lesion Cartilage & subchondral bone status Signal intensity below lesion Tc99m bone scans
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Table 43-7 -- Staging Systems for Osteochondritis Dissecans From Dipaola JD, Nelson DW, Colville MR: Characterizing osteochondral lesions by magnetic resonance imaging, Arthroscopy 7:101, 1991.
Slide 20-

Treatment Non-op Stable lesions Esp. with open physes Activity modification Protected WB Signs of healing after 3-4 months? Progression from rehab to sports/impact activities as tolerated 50% success rate in juvenile cases Lower success rates Larger lesion, skeletal maturity, location other than medial femoral condyle, lesion instability
Slide 21-

Treatment Surgical Indications Failed non-op, unstable lesions, symptomatic in adults Goals: maintenance/restoration of joint congruity and rigid fixation of unstable fragments when possible
Slide 22-

/ Crawford & Safran 2006 JAAOS
Slide 23-

OCD Capitellum May be confused with Panner disease Not associated with trauma Overhead athletes, gymnasts Ruchelsman, et al. (2010) J Am Acad Orthop Surg 18: 557-67 Zlotolow, et al. (2014) JHS
Slide 24-

OCD Capitellum Zlotolow, et al. (2014) JHS
Slide 25-

OCD Capitellum Zlotolow, et al. (2014) JHS
Slide 26-

OCD Talus
Slide 27-

Treatment Surgical procedures Arthroscopic drilling for symptomatic stable lesions Symptomatic stable lesions in juveniles In unstable OCD lesions, any fibrous tissue found at the base of the lesions should be débrided Options for fixation of unstable fragments (still relatively intact and congruous include): Herbert screws Cannulated screws Bioabsorbable pins/screws Options for OCD fragments <2 cm2 in diameter deemed irreparable Marrow stimulation techniques Microfracture Drilling arthroplasty Abrasion arthroplasty Other options OATS Osteochondral allograft reconstruction ACI Crawford, et al. (2006) J Am Acad Orthop Surg 14: 90-100
Slide 28-

Microfracture Considered first line treatment of full thickness cartilage defects Minimally invasive Technical ease Low cost Limited surgical morbidity
Slide 29-

Microfracture Lesion debrided to stable, squared off edges Zone of calcified cartilage is removed Not subchondral bone though Cortical penetration Medullary bleeding/ clot formation Leave 1-2 mm bone bridges Avoid confluence of holes Surgical awl perpendicular to subchondral plate Defect fills with fibrin clot Vertical walls are key: reduces shear and compression
Slide 30-

Microfracture Healing Response Clot formation Undifferentiated (pluripotent) mesenchymal cells in clot mature to yield fibrocartilage repair tissue. Vascular ingrowth Tissue is mainly type I collagen Compared to native hyaline cartilage (type II): Inferior stiffness, poorer wear characteristics than normal hyaline cartilage
Slide 31-

Microfracture Post op Up to 6 weeks of NWB Use of CPM for 6 hours / day Lesion in patellofemoral joint: Wear a brace with flexion stop at 30º to limit patellofemoral contact Weight bearing permitted
Slide 32-

Microfracture Outcomes Steadman et al (Arthroscopy 2003): 80% of 71 knees in patients <45 yrs w/ isolated post-traumatic full thickness chondral defects improved at an average follow up of 7 yrs Literature review of 28 studies with 3122 pts: Clear improvement of knee function at 24 months but inconclusive durability at greater than 24 mos McAdams et al 2009 Am J Sports Med
Slide 33-

Osteochondral Autograft Transplantation (OAT) Harvests viable, structurally intact cartilage and bone plugs from a less valuable portion of the joint, and transplanting to site of symptomatic cartilage injury. Place donor plug flush with articular surface to achieve normal contact pressures over the healed graft Articular gaps fill with fibrous tissue
Slide 34-

OAT Technique Harvest from intercondylar notch or margins of condyles above sulcus terminalis May use a small lateral arthrotomy Patella can interfere w/ arthroscopic harvest Depth of donor site 12-15mm Recipient socket 2mm shorter than donor Donor plug: can match size of defect (<10mm) Donor plug flush with site Centrally direct graft on insertion, via scope
Slide 35-

OAT Postop NWB for 6 weeks CPM for 6 hours per day Progressive WB
Slide 36-

OAT Outcomes Best results for < 2cm2 lesions Good results shown for < 4cm2 lesions Hangody and Fules (JBJS 2003): 831 pts over 10 yrs 92% had good to excellent results for femoral condylar mosaicplasty 79% patellar and/or trochlear mosaicplasty 87% tibial mosaicplasty 94% talar mosaiplasty
Slide 37-

Osteochondral Allograft Transplantation Useful for larger lesions (2-3.5+ cm2) Typically 2nd line tx Tissue matching/immunosuppression Usually not necessary as chondrocytes are isolated by the cartilage matrix Disadvantage: pts must be “on-call” when fresh (<28 days) allograft becomes available Frozen can also be used
Slide 38-

Osteochondral Allograft Technique Similar to autograft Reamer converts defect to a circular recipient socket w/ uniform depth of 6-8mm Pulse lavage before insertion Reduce risk of graft immunogenicity Press fit graft Fixation can be augmented by metal compression screws
Slide 39-

Osteochondral Allograft Post op TTWB first 6 weeks Patellofemoral graft: limited to 45º flexion CPM immediately after surgery
Slide 40-

Autologous Chondrocyte Implantation Ideal for symptomatic, unipolar, well contained defects from 3.5-10 cm2 Two-stage procedure
Slide 41-

ACI Stage 1: Arthroscopic or parapatellar miniarthrotomy Harvest 200-300mg of chondrocytes from nonessential portion of knee (stage I) Specimen sent to Lab Undergoes enzymatic removal of ECM, then culture expansion of chondrocytes Placement in agarose gel
Slide 42-

ACI Stage 2: At least 6 wks after biopsy After preparation of recipient site(s), release tourniquet and achieve complete hemostasis Periosteal patch sewn over defect Cultured cells injected under patch Sealed with fibrin glue
Slide 43-

ACI
Slide 44-

ACI Periosteum: Readily available from proximal medial tibia, distal to pes anserinus insertion At least 2mm larger than defect Contains pluripotent mesenchymal cells Produces chondrogenic growth factors Some porcine substitutes can be used Neocartilage: superficial layer is fibrocartilaginous in nature (“hyaline-like”)
Slide 45-

ACI Post op Restricted WB CPM: 6-8 hours/ day Patellofemoral lesions: full weight bearing in full extension
Slide 46-

ACI Outcomes Good to excellent results in 51 of 61 patients at mean f/u of 7.4 yrs Peterson et al. (Am J Sports Med 2002) Fu et al: (Am J Sports Med 2005): Retrospective cohort comparison of ACI vs arthroscopic debridement for lesions of femoral condyle or trochlea (58 pts) with min 3 yr f/u. Better outcomes with ACI than debridement independent of lesion size Median overall condition Pain Swelling
Slide 47-

Surgical Alternatives for Treatment of Articular Cartilage Lesions - JAAOS 2000
Slide 48-

Comparative Studies Level I & II
Slide 49-

ACI vs OAT Level I prospective randomized clinical trial 58 ACI vs 42 mosaicplasty. Mean 19 mos f/u Good to excellent outcome: 88% ACI, 69% OAT. (p = .277) Subgroups: -Medial femoral condyle: 88% ACI vs 74% OAT (p = .032) -Lateral femoral condyle: 92% ACI vs 40% OAT (p = .182) Key features -Proud placement of OAT plugs, immediate WB for all pts, -no CPM, cylinder cast placement immediately post-op. Arthroscopy @ 1yr (comparing ICRS grade) -82% good to excellent repair tissue in ACI -34% good to excellent repair tissue in OAT Limitations: variety of lesions and anatomic locations, small population, short f/u period, non standard postop protocol
Slide 50-

ACI vs OAT Horas et al. (JBJS 2003) Level II prospective randomized trial 20 pts with ACI & 20 pts with OAT Avg lesion 3.75 cm2 Tighter inclusion criteria Both groups showed improvement Recovery slower in ACI @ 6, 12, 24 months (Lysholm score) Equal Meyers and Tegner activity scores Limitations Insufficient power, inadequate follow-up (less than 80% at 2 yrs), absence of control group
Slide 51-

ACI vs Microfracture Level 1 randomized controlled study. 40 ACI vs 40 microfracture, 12, 24 mos f/u Significant improvement in both groups: ACI (p=.003), microfracture(p=.0001) At 2 yr f/u, no sig difference btw groups based on Tegner, Lysholm, visual analog scores Microfracture improved more based on SF-36 physical component 2nd look arthroscopy (76% of patients): No difference btw groups based on ICRS grading system No significant differences in biopsy Author’s conclusions: ACI and microfracture provided equal results over 2 yrs Younger & more active pts had better outcomes in both groups
Slide 52-

ACI vs Microfracture Knutsen et al. (JBJS 2007) 5 yr Follow-Up of previous study No significant differences between groups 9 failures in each group 1/3 of each group had radiographic OA at 5 yrs post-op
Slide 53-

CCI vs Microfracture Saris et al. (Am J Sports Med 2008) CCI = characterized chondrocyte implantation Designed to select for chondrocytes that express a marker profile more predictive of capacity to form hyaline-like cartilage 57 CCI vs 61 Microfracture pts Both groups had clinically similar results at 6, 12, & 18 months Biopsy at 1 year Superior structural regeneration in CCI vs Microfracture Improved longer-term outcomes?
Slide 54-

OAT vs Microfracture Level I prospective randomized study. 28 OAT vs 29 microfracture All were regional/national athletes in Lithuania – avg age 24.3 yrs Avg 4.3 plugs in Microfracture Avg f/u 37 mos Both groups showed improvement of HSS score -OAT: from 77.99 to 91.08 (p<.0001) -Microfracture: from 77.22 to 80.60 (p<.05) Good to excellent results in 96% OAT and 52% microfrx OAT: sig better results than microfrx at 1,2,3 yrs postop. 9 failures in microfrx group vs 1 failure in OAT group. Worse Outcomes Age > 30 yrs Microfracture for lesions > 2 cm2
Slide 55-

102 randomized to OAT, microfracture or debridement + ACL Matched control group with intact cartilage + ACL All 4 groups significantly improved OAT significantly better than microfracture and debridement Intact cartilage significantly greater than OAT
Slide 56-

Conclusions Comparative studies have not demonstrated superiority of ACI vs OAT Microfracture may be as good as ACI Arthroscopic OAT seems to provide better outcome than microfracture specifically for initial treatment of young athletes Microfracture considered best first line tx overall, for full thickness articular cartilage lesions. Can be performed without a 2nd procedure and without an arthrotomy No level I studies using a true natural history control group.
Slide 57-

Comprehension Quiz
Slide 58-

(SBQ07-32) A patient with a symptomatic chondral defect undergoes the arthroscopic procedure seen in Figure A. The reparative tissue would best be described as which of the following? FIGURES: A 1. Fibrocartilage2. Fibrous tissue3. Elastofibroma 4. Hyaline cartilage5. Chondromalacia
Slide 59-

PREFERRED RESPONSE ▼ 1 The figure is an arthroscopic photo of a microfracture procedure, which creates a reparative tissue best described as fibrocartilage. Microfracture is a marrow stimulation technique where stem cells from the medullary canal are given access to the base of the lesion by making small perforations in the subchondral bone. The rationale for this technique is based on these stem cells differentiating into cells that will produce an articular cartilage repair. However, biopsy findings in animals and humans have demonstrated primarily a fibrocartilagenous repair tissue and not true articular cartilage regeneration. The collagen type found in hyaline or articular cartilage is of the type II variety. Fibrocartilage possesses some type II, but is mostly type I and III cartilage. Both the Intructional Course Lecture and the textbook by Buckwalter provide an in-depth review of articular cartilage biology and the background for chondral resurfacing techniques.Incrorrect Responses:2. Fibrous tissue is created by fibrocytes and lacks type II collagen.3. Elastofibroma is a distractor (elastofibroma dorsi is a fibrous tumor with a predeliction for the scapulothoracic joint).4. Hyaline cartilage is true articular cartilage with predominantly type II collagen. It also has columnar organization and a lamina splendens (which differentiates it from what has been called hyaline-like tissue).5. Chondromalacia refers abnormal softening of the cartilage and is a common pathologic condition of the the knee. References: 2) Buckwalter JA, Mankin HJ: Articular cartilage: Degeneration and osteoarthritis, repair, regeneration, and transplantation. Instr Course Lect 1998;47:487-504 3) Buckwalter JA, Einhorn TA, Simon SR (eds): Orthopaedic Basic Science: Biology and Biomechanics of the Musculoskeletal System, ed 2. Rosemont, IL, American Academy of Orthopaedic Surgeons, 2000, pp 471-488
Slide 60-

(OBQ10-257) Following a medial femoral condyle osteochondral autograft mosaicplasty, which of the following statements best describes the fixation of the graft? 1. Graft fixation strength increases linearly with time until subchondral union at 3 months2. Graft fixation strength initially decreases during the early healing phase, and then increases with subchondral bone healing3. Graft fixation strength does not change during the first 3 months following surgery4. Graft fixation strength is enhanced by early weight bearing5. Graft fixation strength initially increases over the first 6 weeks, then recedes with bony remodeling
Slide 61-

PREFERRED RESPONSE ▼ 2 Following mosaicplasty, appropriate post-operative rehabilitation and weight-bearing status must be based upon the fixation of the osteochondral autograft plugs. Whiteside et al performed a porcine study evaluating the fixation strength of osteochondral autograft mosaicplasty during the first week following implantation. The graft fixation was notably weaker one week following surgery due to the post-operative response and host remodeling. These results suggest that protected weight bearing should be used until the osteochondral plugs have healed into the subchondral bone, generally by 3 months. However, early non-weight bearing motion is important to prevent stiffness and protect the joint surfaces with synovial fluid. References: 2) Tyler TF, Johnson C, Jenkins WL. Rehabilitation following osteochondral injury to the knee.nee. Orthopaedic Knowledge Update: Sports Medicine 4. Rosemont, IL: American Academy of Orthopaedic Surgeons; 2009:257-262. 3) Whiteside RA, Bryant JT, Jakob RP, Mainil-Varlet P, Wyss UP. Short-term load bearing capacity of osteochondral autografts implanted by the mosaicplasty technique: an in vitro porcine model. J Biomech. 2003 Aug;36(8):1203-8. PMID:12831747 (Link to Abstract)
Slide 62-

(OBQ08-94) A 32-year-old female is referred to you for definitive treatment of a symptomatic focal chondral defect on her medial femoral condyle. A photograph from a recent diagnostic arthroscopy shows the defect (Figure A), which measured 20 x 25mm after debridement. What surgical treatment would you reccomend? FIGURES: A 1. Osteochondral autograft2. Osteochondral allograft3. Microfracture4. Chondroplasty5. Abrasion arthroplasty
Slide 63-

PREFERRED RESPONSE ▼ 2 Based on the age of this patient and the size of this lesion (2 x 2.5 = approx 5cm square) an osteochondral allograft plug is the best choice. The results of microfracture are better for contained defects less than 2cm square. Autografts are generally reserved for smaller defects as well because harvesting enough plugs to fill this defect may lead to significant donor site morbidity. Chondroplasty and abrasion arthroplasty are not good solutions to this chondral defect in a young symptomatic patient. Autologous chondrocyte implantation (ACI) would also be a correct response, but it was not listed.Bert discusses the science, histology, history, and clinical results of abrasion arthroplasty for treatment of osteoarthritis of the knee. Alford et al. review the indications for treatment of chondral defects and describe the various treatment options. In addition, they discuss clinical scenarios regarding comorbid conditions including ligament instability, meniscal deficiency, and malalignment by developing a treatment algorithm (Illustration A).