On-line CEUs

NAOT members with an active OTC credential can earn CEU credits toward recertification just by reading the “Tip of the Month” contained in each issue of the Orthotech Professional and answering a few short questions at the conclusion of the article.  Members can either answer the questions in the print version of the newsletter and return them via fax or mail to the NAOT offices, or submit answers on-line by clicking on the link at the end of each article and completing the on-line questionnaire. To receive 1 CEU (Category 2) for each article read, you must include:

-Your full name
-NAOT member number
-Email address (if applicable)
-Answers to all questions
-OTC number 

Articular cartilage injuries are the cause of significant musculoskeletal morbidity for both the young and aging population. Articular cartilage lesions can be located on one focal aspect of the tibiofemoral or patellofemoral joint, or can be very large and involve many compartments of the knee, often referred to as osteoarthritis. Currently surgical treatment options offer reparative, and restorative treatment strategies. The purpose of this article is to discuss the basic science of articular cartilage, current treatment options available, and the rehabilitation protocols for each treatment and progression post-surgically.

Articular cartilage defects can be limited to the superficial layers of the cartilage or can extend to the underlying subchondral bone, partial versus full thickness defects. An articular cartilage lesion is defined as any injury to the articular cartilage that causes softening, fissuring, and fibrillation to the articular cartilage. Bone bruises and other abnormal findings on MRI or bone scans represent an alteration in the healthy state of articular cartilage and should be treated as a risk factor for future potential articular cartilage degeneration (Kevin E. Wilk, 2006).

While symptomatic, small full-thickness injuries may be successfully treated with minimally invasive techniques, large defects may respond poorly to such techniques and may require more sophisticated strategies. Articular cartilage degeneration of the knee joint also referred to as osteoarthritis. Osteoarthritis occurs more commonly in the middle to later aged individual and often causes a sedentary lifestyle as a consequence (Paul B. Lewis, 2006). Articular cartilage is hyaline in nature. Hyaline cartilage is composed of both a solid and fluid phase. The interaction of these two phases provides specific biphasic viscoelastic properties. The solid phase of cartilage is composed of collagen and proteoglycans, together forming the extracellular matrix of the articular cartilage. Collagen interacts to form large fibrils that trap large proteoglycan aggregates. The proteoglycan aggrecan is the protein backbone containing both chondroitin sulfate and keratin sulfate. Water comprises up to 60-80% of the total weight of the tissue. Interaction of water with proteoglycans provides a swollen, hydrated tissue that resists compression. Chondrocytes are sparsely distributed throughout the matrix and provide only 2% of the total volume of articular cartilage. Chondrocytes maintain the extracellular matrix surrounding them and are imperative for maintaining healthy cartilage. Chondrocyte survival depends on physical stresses, and electrostatic forces (Paul B. Lewis, 2006).

Hyaline cartilage is organized histologically into four specialized layers each providing unique characteristics and structure. These layers include superficial to deep include, the superficial layer (tangential zone), the middle layer (transitional zone), the deep layer (radial zone), and the calcified layer (calcified cartilage). The superficial layer protects the deeper layers from the shear stresses of articulation. Just deep to the superficial layer is the transition zone, providing an anatomic and functional bridge between the superficial and deep zones. This layer is the first line of resistance to the compressive forces found in the deep zone. The bulk of resistance to compressive forces is found in the deep zone, where collagen is organized perpendicular to the articulating surface. The calcified layer plays a very important role in securing the cartilage to the bone (Paul B. Lewis, 2006).

The articular cartilage of the knee can be damaged as a result of many mechanisms including direct blunt trauma, indirect impact loading, and torsional loading. There are also many factors associated with articular cartilage degeneration including direct trauma, obesity, immobilization, and excessive repetitive loading. Sport activities alone do not appear to be risks in the normal knee (Kevin E. Wilk, PT, DPT, 2004).

Articular cartilage has limited ability for repair because of its relatively avascular nature and apparent lack of chondrocyte division and migration around and into the zone of injury. In the early stages of partial thickness injuries, the injured chondrocytes have impaired metabolic capacity and cannot maintain the normal proteoglycan concentration, leading to increased tissue hydration and disorganization of the collagen. Biomechanically, this causes increased force transmission to the subchondral bone, causing impact loads to be more readily transmitted to the damaged cartilage. Chondrocytes can only respond by proliferating and increasing the production of matrix molecules at the site of the injury, however this new matrix typically fails to restore the native surface. This degeneration is thought to contribute to the progression of partial-thickness lesions (Paul B. Lewis, 2006).

Full-thickness injuries that penetrate the subchondral bone theoretically have a higher potential for intrinsic repair. The localized bleeding created by disrupting the subchondral bone provides for hematoma formation and a primitive healing response. Stem cells produce type I collagen fibers to fill the full-thickness defect with fibrocartilage, providing the necessary functions needed of articular cartilage. Fibrocartilage matrix has inferior stiffness, resilience, and wear qualities (Paul B. Lewis, 2006). The absence of intrinsic healing capacity in articular cartilage has led to the development of multiple operative strategies for addressing focal chondral defects. Individuals with high physical demands require a careful, stepwise approach that includes reparative and restorative strategies. Reparative strategies utilize marrow stimulation techniques to induce formation of fibrocartilage. Restorative tactics attempt to replace damaged cartilage with hyaline or hyaline-like tissue using osteochondral or chondrocyte transplantation (Paul B. Lewis, 2006).

Microfracture Procedure

Figure 1: Steps of the microfracture technique: Left: Damaged cartilage is removed. Center: Awl is used to make holes in the subchondral bone. Right: Healing response brings new, healthy cartilage cells.

The microfracture procedure is a reparative technique to stimulate the underlying marrow, which, in turn, may lead to a stereotyped vascular response to injury (Thomas J. Gill, 2006). The microfracture procedure begins with debridement of the lesion, using a curette, of all remaining cartilage and scar tissue to establish a well defined edge. A surgical awl is then used to perforate the subchondral plate, creating holes spaced two to three millimeters apart, working from the periphery to the center of the defect (Paul B. Lewis, 2006). Once the microfracture is complete, the arthroscopic pump is turned off to make sure that marrow bleeding is observed flowing from the small holes and filling the defect (Figure 1) (Thomas J. Gill, 2006).

Following penetration of the subchondral plate, a biologic response is stimulated. This biological response has three phases beginning with necrosis. Necrosis begins immediately after injury and is characterized by varying degrees of tissue death, depending on the severity of the trauma and the adequacy of the blood supply. The inflammatory phase then kicks in, and is mediated by the local vasculature. A dense fibrin network is formed at the site of the injury, which is rich in inflammatory cells with the potential for cell division and the possibility for repair. This fibrin network is then invaded by neovascularization, causing the inflammatory cells to modulate into fibroblasts, which produce loose granulation tissue. This granulation tissue ultimately matures into a fibrous repair matrix, and finally a scar. The remodeling phase then tries to recreate normal anatomy (Thomas J. Gill, 2006).

Postoperative management is as important as the actual surgery, and compliance with the postoperative rehabilitation program is essential to the outcome of the procedure. Most surgeons recommend a period of restricted weight bearing after the microfracture procedure to protect the healing of the cartilage. The rehabilitation protocol for the microfracture procedure is four phases; the protection phase (weeks 0-5), the intermediate phase (weeks 5-8), the light activity phase (weeks 8-16), and the return to activity phase (weeks 16-26) (Kevin E. Wilk, PT, DPT, 2004).

After surgery, the patient will be in a hinged knee brace locked at 0 degrees extension. The patient is only allowed to come out of the brace to use their Continuous Passive Motion machine, set at 1 cycle per minute, using the largest range of motion that the patient finds comfortable (Thomas J. Gill, 2006).

The goals of the protection phase are to reduce swelling and inflammation, protect and promote healing of the articular cartilage, restore full passive knee extension, gradual restoration of knee flexion, and re-establish voluntary quadriceps control. In the protection phase, ice and compression are used 6-8 times daily for inflammation control. The patient is non weight bearing for the first two weeks, with the use of crutches to control weight bearing forces. At week three, the patient can progress to toe-touch weight bearing, and can progress to 25% weight bearing on week four.

At Week 5, the patient progresses to the intermediate phase, with goals of protecting and promoting articular cartilage healing, gradually increasing joint stresses and loading, improving lower extremity strength and endurance, and gradually increasing functional activities. The patient can progress weight bearing to 50% at Week 6, and 75% at Week 7. Progression through this phase is based on monitoring patient swelling, pain, and motion.

Weeks 8-16 are the light activity phase, looking to improving muscular strength and endurance, increase functional activities, gradually increase loads applied to the joint, and control compression and shear forces. Criteria to progress to phase III are; 1. Patient has full non-painful range of motion, 2. Patient strength is within 20% of the unaffected limb, and 3. Patient is able to walk 1.5 miles or bike 20-25 minutes without symptoms. The patient will gradually progress to the return to activity phase, with a physician approval and is very patient specific.

Osteochondral Grafting: Osteochondral Autograft and Allograft Transfer

Figure 2: Osteochondral Autograft Transfer: Left: Removal of the plug; Center: The new osteochondral plug being placed; Right: After the plug is placed and the new surface cartilage is intact.

An osteochondral autograft procedure is indicated for symptomatic, unipolar lesions of the distal femoral condyle in a nondegenerative joint that has proper limb alignment, as well as ligamentous stability and meniscal competence (Paul B. Lewis, 2006). The objective of an osteochondral autograft transfer is to take healthy articular cartilage from a minimally load-bearing region of the knee and transfer it to the damaged region of the same knee in a single procedure. The osteochondral autograft transfer is all-arthroscopic, the donor plug is harvested typically from the femoral intercondylar notch, the graft is harvested through the use of standardized graft harvesters, placed perpendicular to the donor site, and advanced 12-15mm into the cartilage and underlying subchondral bone, the harvester is then rotated to extract the donor osteochondral plug. Preparation of the recipient tunnel is prepared similarly, except the hole is created at a depth of 2mm less than the donor graft. After the recipient tunnel is prepared, the donor graft is press-fit atraumatically and seated with the use of a tamp so that it lies flush with the surfaces of the neighboring cartilage (Figure 2).

Similar to an autograft transfer, is an osteochondral allograft transfer using tissue taken from cadaveric donors. The techniques are very similar, and have benefits and drawbacks. Benefits for the allograft procedure are elimination of donor site morbidity and ability to provide fully formed articular cartilage without specific limitation with respect to defect size. The drawbacks to the procedure are graft availability, cell viability, immunogenicity, and risk of disease transmission (Paul B. Lewis, 2006).

After surgery, the patient will be in a hinged knee brace (Appendix A) locked at 0° during weight bearing activities and will have to sleep in the locked brace for the first 2-4 weeks. Goals during the protection phase of rehabilitation (week 0-6) will be to protect the healing tissue from load and shear forces, decrease pain and effusion, restore full passive knee extension, gradually improve knee flexion, and regain quadriceps control. Use of a CPM machine (Appendix B) will be initiated on day 1 for 8-12 hours a day (0-40°) for 2-3 weeks. The patient will be instructed to progress the CPM range of motion 5°-10° per day, and may continue to use the machine for 6-8 hours a day for up to 6-8 weeks. Ice, elevation, compression, and edema modalities are also recommended as needed for edema control.

Weight bearing progression for osteochondral autografts are as follows: brace locked during ambulation for 2-4 weeks post-surgery, with the use of crutches for ambulation. Weeks 0-2 non-weight bearing, Week 3-4 toe-touch weight bearing, week 5-6 50-75% partial weight bearing, and week 6-8 full weight bearing allowed. Range of motion progression; Week 1, 0-90°, Week 2, 0-105°, Week 3, 0-115°, Week 6, 0-125°, Week 7-8, 0-135°. Patients with osteochondral autografts have similar rehabilitation exercise progression as the microfracture. Patients will begin to return to low impact sports at month 4-5, moderate impact sports at month 5-6, and high impact sports at month 6-9. Patients undergoing the osteochondral allograft procedure have a similar rehab progression as those having the autograft, yet it is slightly slower due to allograft tissue taking longer to incorporate. The patients are non-weight bearing for 6-8 weeks, and full weight bearing at Week 10-12 (Kevin E. Wilk, PT, DPT, 2004).

Autologous Chondrocyte Implantation (ACI) Procedure

Figure 3: Steps of an Autologous Chondrocyte Implantation Procedure (ACI).

The Autologous Chondrocyte Implantation (ACI) is used to treat large, full-thickness chondral injuries. The principle behind using autologous chondrocyte is to produce a repair tissue that more closely resembles the morphologic characteristics of hyaline cartilage and is therefore better able to restore the durability and natural function of the knee joint (Scott D. Gillogly, 2006). The primary indications for ACI are symptomatic, large, full-thickness chondral lesions located on the femoral chondyles and trochlear groove in patients ranging in age from adolescence to their fifties. The patients must also understand and be willing to comply with the postoperative rehabilitation protocol.

The surgical technique includes two stages, the first stage involves an arthroscopic procedure to obtain a chondral biopsy for growing the autologous chondrocytes and the second is an open procedure for the implantation of the cells within the chondral defect. The biopsy is obtained from the superior peripheral edges of the lateral or medial femoral chondyles or from the inner edge of the intercondylar notch (Scott D. Gillogly, 2006).

All damaged and unhealthy-appearing cartilage and fibrocartilage is removed during debridement of the defect, leaving exposed subchondral bone with a rim of stable cartilage. Overly aggressive debridement is avoided so as not to enter the cancellous portion of the bone, which would create excessive bleeding within the defect. The next step is to obtain a periosteal graft to be transferred to the defect and secured to contain the cells. The periosteal graft is then aligned over the defect, sutured to the cartilage rim, and sealed with fibrin glue. The autologous chondrocytes are then sterilely injected under the periosteal graft into the defect. The injection site is then closed with additional sutures and sealed with fibrin glue, completing the ACI procedure (Scott D. Gillogly, 2006) (Figure 3).

After surgery is complete, a knee immobilizer is applied to the patients knee. The rehabilitation program following an ACI procedure is vital to the success and long-term outcomes. The concept of slow, gradual maturation of the repair tissue is crucial to understanding the rehabilitation following an ACI. The patients hinged knee immobilizer will be locked at 0° during weight bearing activities and will sleep in the locked brace for 2-4 weeks. The patient is non-weight bearing for 1-2 weeks, and may begin toe-touch weight bearing immediately per physician or at Week 2-3. Partial weight bearing is initiated at Week 4-5. The patient will begin the CPM machine on day 1 for a total of 8-12 hours a day (0-40°) for 2-3 weeks, and will progress the CPM ROM as tolerated 5°-10° a day. Patellar mobilization is recommended 4-6 times per day. The biologic nature of the hyaline-like repair tissue must be both protected and stimulated to allow the maturation and remodeling of the tissue. Premature overload of the repair tissue will increase the likelihood of failure (Scott D. Gillogly, 2006).

The ACI rehabilitation guidelines are broken down into IV phases, and are very specific. At the end of each rehabilitation phase, the guidelines specify what goals the patients have to have met in order to progress to the next phase. In order to progress to phase II (Transition Phase), the patient must be at least 6 weeks post-surgery and have full passive knee extension, 120° of knee flexion, have minimal pain and swelling, and have gained voluntary quadriceps activity. To progress to phase III (Maturation Phase), the patient must be 12 weeks post-surgery and have full range of motion, have acceptable strength levels (Hamstrings 10-20% contralateral leg, Quadriceps 20-30% of contralateral leg), be able to pass a balance test within 30% of the contralateral leg, and be able to walk 1-2 miles or bike 30 minutes. In order for the patient to progress to the final phase IV (Functional Activities Phase), the patient must have full non-painful range of motion, strength within 80-90% of their contralateral extremity, have balance and/or stability within 75% of their contralateral extremity, and have no pain, inflammation, or swelling.

The variegated structure of hyaline cartilage makes treatment of cartilage injuries for the scientist, surgeon, and physical therapist problematic. Recent advances in the science of cartilage restoration on both the basic science and clinical levels have led to the development of a variety of treatment options depending on the patient, activity level and the patients’ outcome expectations. Arthroscopic debridement may be an appropriate procedure for certain patient populations with low physical demands. Reparative techniques such as microfracture and restorative techniques such as osteochondral autograft transfer are appropriate treatment options for higher-demand individuals with small, contained chondral lesions. The autologous chondrocyte implantation and osteochondral allograft transplantation are appropriate for higher-demand individuals with larger chondral lesions or those with significant involvement of the subchondral plate. These operative techniques rely upon a time-dependent maturation and remodeling of repair tissue for their success, therefore the importance of post-operative care is crucial in the outcome of the surgical procedure and the patients return to their ‘normal’ daily activities.