Skip Navigation LinksHome » Articles » Articular cartilage defects in the knee

Articular cartilage defects in the knee

Postoperative rehabilitation


– Written by Barbara Wondrasch, Austria


Focal articular cartilage defects in the knee joint are highly prevalent and are a common cause of functional restrictions and pain during daily life and sport activities1,2,3. Treatment of these defects presents a clinical challenge for physicians and physiotherapists for two reasons. Firstly, this type of articular cartilage defect typically affects young active individuals in their mid-twenties to late thirties, who have high demands on their knee function. These individuals may be active sports participants and/or have an active or strenuous job4. Secondly, the nature of articular cartilage tissue – being avascular and aneural – prevents the physiological inflammatory response to tissue injury. This results in a repair tissue that is both qualitatively and quantitatively insufficient and incapable of meeting the demands of these active individuals5.


To address focal cartilage lesions in the knee, reparative and restorative surgical treatment techniques are preferred. These techniques can be summarised by the term ‘cartilage repair’, as these techniques emphasise stimulation of the healing process in repair tissue. The most common techniques include microfracture, osteochondral grafts and autologous chondrocyte implantation (ACI)6,7.


Surgeons and physiotherapists generally agree that rehabilitation after cartilage repair in the knee is critically important, with the potential to influence both patient outcome and the quality of repair tissue8,9. However, good quality research to support these assumptions is lacking, with most of the rationale for rehabilitation after cartilage repair based on expert opinion, applied biomechanics and basic science9-16. Ideally, physiotherapists should implement an effective and individualised, but safe rehabilitation protocol that is built on evidence-based research and science8. This article will describe the fundamental principles of postoperative rehabilitation after cartilage repair and will present the most important components of rehabilitation protocols after cartilage repair in the knee.



There are several factors which influence the quality of the repair tissue and patient outcomes, including: successful cell culturing under good practice conditions, expertise and technical proficiency of the surgeons, patient compliance to a pre- and postoperative treatment regime and a safe, but progressive, postoperative rehabilitation programme8,17.


The World Health Organisation has established the International Statistical Classification of Diseases and Related Health Problems (ICF), which classifies health and health-related domains into several levels, including a list of body functions, body structures and a list of domains of activity and participation18,19. Based on this classification, rehabilitation after cartilage repair aims to provide a mechanical environment for the local adaption and remodelling of the repair tissue (body functions and structures) and to restore joint range of motion (ROM) and muscle control (body functions). Further, it should be ensured that patients can safely return to an optimal level of knee function to perform activities such as walking and stair climbing (activities) to be able to participate safely in day to day activities, including working, social, recreational and sporting activities (participation).


A ‘safe’ return to activity requires a thorough understanding of the biological and biochemical factors that are inherent in the respective cartilage repair techniques. Further, the biomechanics of the affected joint needs to be considered to appreciate the forces that will be exerted on the defect area8,10. Generally, an individual approach should be emphasised, addressing factors such as age, body mass index, number of previous surgeries, duration of symptoms and activity level8,9.



The process of rehabilitation after cartilage repair is guided by three biological healing phases independent of the inherent and specific differences between surgical cartilage repair procedures:

  1. Initial protection and activation
  2. Loading and functional restoration
  3. Activity restoration9.

The first phase, protection and activation, is characterised by graft integration and stimulation of the chondrocytes. During the second phase, loading and functional restoration, matrix production is at its peak, with organisation of the collagen fibres. The focus of the third phase, activity restoration, is maturation and adaptation of the healing repair tissue9,20.


The biological mechanism in the protection and activation phase differs between the particular surgical techniques. With microfracture and ACI the cells contained in the defect start to differentiate and produce a soft and unorganised initial repair tissue, which is very vulnerable to mechanical overload and requires protection. Osteochondral grafting also needs protection to allow for an adequate bone-to-bone healing of the implanted grafts. As bony healing is less vulnerable to mechanical damage compared to cartilage growth, progression of weight bearing (WB) and WB activities in the protection and joint activation phase is usually faster with osteochondral grafting compared to microfracture and ACI. However, high shear and compressive forces in the first rehabilitation phase may negatively influence chondrocyte metabolic rate and tissue repair and integration of all three of these repair procedures. In contrast, low mechanical stimulus may support the development of cartilage tissue by promoting cartilage formation, nutrition and bone-to-bone healing. Hence, the challenge of the protection and joint activation phase is to provide appropriate stimulation of the healing tissue while avoiding deleterious forces which might jeopardise the healing process9,21,22.


From a biological point of view, the aim of the loading and functional restoration phase is to increase the mechanical load to stimulate the chondrocytes’ metabolism – leading to extracellular matrix (proteoglycans, collagen fibres) production. Mechanical load should be gradually increased to strengthen the healing tissue as it becomes more resilient to increased loading activities9,23. However, the increase of mechanical stimulus and loading should be performed in a controlled and progressive manner to avoid excessive overload which might damage the healing tissue9.


The activity restoration phase is characterised by further organisation and maturation of the healing cartilage tissue with increased rigidity of the extracellular matrix due to further proteoglycan deposition, collagen production and cellular organisation7,24. Gradually increased impact and sport-specific movement patterns prepare patients to return to the higher mechanical stress associated with sport activities9.



An understanding of applied clinical biomechanics and an appreciation of the forces that will be exerted on the healing tissue are essential in the design of rehabilitation programmes after cartilage repair. The contact area (distribution and magnitude), contact load and contact pressure during rehabilitation should be considered to minimise the danger of damaging the healing tissue and support the healing process by physiologically stimulating the tissue10. Therefore, information from the surgeon on the nature of the defect (size and location) is crucial. With this information, rehabilitation modalities and exercises can be incorporated in safe ranges, while avoiding ranges which might be detrimental to the healing tissue8.


The flexion and extension movement within the tibiofemoral joint is a combination of rolling and gliding of the surface of the femur and the tibia, combined with a rotational movement at the end of flexion and extension. To ensure a flexion and extension movement with a physiological load distribution on the cartilage surfaces, restriction of these rolling, gliding and rotational movements should be avoided. During this extension and flexion only parts of the tibia and femur are articulating25, thus, the load distribution in the tibiofemoral joint should be considered when progressing exercises. The tibiofemoral joint is exposed to high mechanical load during vertical WB activities (for example during walking, standing and stair climbing)26, which should therefore be avoided in the early protection phase.


The patellofemoral joint is a sellar joint composed of the patella and the underlying femoral trochlea. This joint is stabilised by active and passive stabilisers; the major active stabiliser is the quadriceps muscle, whereas passive stabilisation is provided by the femoral condyle, the peripatellar retinaculum, and the medial and lateral patellofemoral ligaments26,27. At higher knee flexion angles, particularly in WB positions, the load within the patellofemoral joint increases, implying increased loading of the healing cartilage tissue. However, near to extension, the load within the joint is low28,29. Hence, WB activities with the knee in an extended position are possible without harming the repair tissue – a brace can be used to lock the knee in an extended position.



Despite the understandable ambition for a standardised rehabilitation programme, the individuality of each patient has to be considered. Several factors have been identified that should influence the rehabilitation programme. These factors include the nature of the defect (size and location), patient age, body mass index, number of previous injuries, activity level and the demand the patient usually places on their knee8,9,30. Table 1 presents these factors and their possible influence on the rehabilitation process.



The duration of each phase and its rehabilitation modalities might vary between the different cartilage repair techniques due to inherent biological and biochemical differences. Progression through the rehabilitation phases should be based on criteria rather than fixed timelines, however several rehabilitation modalities and the progression within the rehabilitation programme should be based on the biology of the healing tissue9.


Pain and effusion, two optimal indicators for overloading of the joint and the healing tissue, should guide the rehabilitation process and must not be ignored. The phases, including possible rehabilitation modalities, are presented in Table 2.


Phase 1: protection and activation phase

The focus of the first phase of the rehabilitation programme should be on reducing effusion and pain, restoration of ROM, regaining muscular and neuromuscular control, as well as monitoring WB restrictions9-11.


A primary goal of this first postoperative phase is to reduce pain and effusion. It is well known that pain and swelling can lead to quadriceps inhibition with concomitant negative effects on joint biomechanics, neuromuscular control and increased joint reaction forces. Further, decreased quadriceps activity can result in reduced active ROM, particularly in a loss of active extension31,32. Additionally, increased intra-articular joint temperature can activate proteoglytic enzymes, which have been shown to have a detrimental effect on both healthy and healing cartilage tissue5.


The amount of initial WB and the progression of WB activities have to be determined based on the cartilage repair technique and individual factors (age, body mass index, neuromuscular control, associated surgical interventions). Patients have to be instructed to use crutches to reduce WB, this should be regularly assessed using standard bathroom scales9,10,33. The regular assessment is important, as it has been shown that patients do not reliably adhere to the given WB instructions34. Microfracture and ACT have historically required longer periods of WB restrictions with a slower progression compared to osteochondral grafting9. Table 3 presents common WB restrictions.


A further main component of this phase is the restoration of joint ROM, as a normal ROM is the first step towards normalisation of joint arthrokinematics, which is essential to provide physiological loading of articular cartilage tissue. Cyclic dynamic movements in the available ROM in non-WB positions support mechanical stimulation of the cells and increases synovial fluid and nutrition to the healing tissue35,36. Active and passive ROM exercises should be performed in closed kinetic chains (CKC) to prevent shear forces over the repair site8,37 as well as pain and effusion.


Muscular activation is a key factor in restoring muscular joint control and normal arthrokinematics. Further, development of muscle strength and endurance is important to distribute forces acting on the knee and to protect the healing site. Muscle strengthening exercises aim at optimising joint loading through improving alignment and the capabilities of the muscles to absorb shock during activity. In particular, quadriceps and hamstring strengthening exercises should be emphasised to restore lower extremity muscle strength and to actively stabilise the knee joint. In addition, the hip muscles (gluteals) play a major role in providing functional joint alignment by preventing lower extremity dynamic valgus8,10,38. In this first phase, isometric and CKC exercises outside of the defect zone are recommended, as they produce no shear forces and damage to the healing tissue can be avoided8,9.


Furthermore, proprioceptive deficits should be addressed in this phase by the implementation of neuromuscular exercises which should be performed within the patient’s WB restrictions8,9.


Phase 2: loading and functional restoration phase

The main focus of this second phase is a controlled, but progressive, increase of WB activities. This can be achieved by increasing joint ROM, restoring muscular and neuromuscular control and the beginning of more complex movement patterns, which require proper dynamic joint stability. The ability to generate a sufficient amount of force in a timely fashion is of significance to maintain dynamic stability of the knee and limit excessive joint motion that may affect the static structures such as ligaments and cartilage26,39. Core strength has also been shown to have a significant impact on the loading of the lower extremity40-42. In this phase concentric and eccentric muscle strength training should be emphasised to provide dynamic knee stability. However, this should be done in safe ranges to minimise the danger of jeopardising the healing graft and ensure no increase in symptoms occurs. Neuromuscular exercises can shift from partial WB positions to full WB and the use of additional weight is possible. Both muscle strength and neuromuscular training should be integrated into complex movement pattern exercises and functional tasks. It is still crucial to be cautious that no increase in symptoms occurs during or after the exercises.


Phase 3: activity restoration phase

This phase aims to prepare the patient to return to higher mechanical stress associated with sports activity. A programme should be developed that allows a continued recovery and meets the biomechanical and physiological demands of the respective sport activities. Further, any remaining muscle strength deficits and additional impairments related to metabolic capacity, sport-specific movement patterns and symptoms should be addressed to provide a safe return to sport9.



Barbara Wondrasch P.T., Ph.D.

Lecturer and Researcher

St. Poelten University for Applied Sciences

St. Poelten, Austria





  1. Aroen A, Loken S, Heir S, Alvik E, Ekeland A, Granlund OG et al. Articular cartilage lesions in 993 consecutive knee arthroscopies. Am J Sports Med 2004; 32:211-215.
  2. Curl WW, Krome J, Gordon ES, Rushing J, Smith BP, Poehling GG. Cartilage injuries: a review of 31,516 knee arthroscopies. Arthroscopy 1997; 13:456-460.
  3. Flanigan DC, Harris JD, Trinh TQ, Siston RA, Brophy RH. Prevalence of chondral defects in athletes' knees: a systematic review. Med Sci Sports Exerc 2010; 42:1795-1801.
  4. Wilk KE, Briem K, Reinold MM, Devine KM, Dugas J, Andrews JR. Rehabilitation of articular lesions in the athlete's knee. J Orthop Sports Phys Ther 2006; 36:815-827.
  5. Alford JW, Cole BJ. Cartilage restoration, part 1: basic science, historical perspective, patient evaluation, and treatment options. Am J Sports Med 2005; 33:295-306.
  6. Lewis PB, McCarty LP 3rd, Kang RW, Cole BJ. Basic science and treatment options for articular cartilage injuries. J Orthop Sports Phys Ther 2006; 36:717-727.
  7. Tetteh ES, Bajaj S, Ghodadra NS. Basic science and surgical treatment options for articular cartilage injuries of the knee. J Orthop Sports Phys Ther 2012; 42:243-253.
  8. Edwards PK, Ackland T, Ebert JR. Clinical rehabilitation guidelines for matrix-induced autologous chondrocyte implantation (MACI) on the tibiofemoral joint. J Orthop Sports Phys Ther 2014; 44:102-119.
  9. Mithoefer K, Hambly K, Logerstedt D, Ricci M, Silvers H, Della Villa S. Current concepts for rehabilitation and return to sport after knee articular cartilage repair in the athlete. J Orthop Sports Phys Ther 2012; 42:254-273.
  10. Hambly K, Bobic V, Wondrasch B, Van Assche D, Marlovits S. Autologous chondrocyte implantation postoperative care and rehabilitation: science and practice. Am J Sports Med 2006; 34:1020-1038.
  11. Hirschmuller A, Baur H, Braun S, Kreuz PC, Sudkamp NP, Niemeyer P. Rehabilitation after autologous chondrocyte implantation for isolated cartilage defects of the knee. Am J Sports Med 2011; 39:2686-2696.
  12. Hurst JM, Steadman JR, O'brien L, Rodkey WG, Briggs KK. Rehabilitation following microfracture for chondral injury in the knee. Clin Sports Med 2010; 29:257-265.
  13. Nho SJ, Pensak MJ, Seigerman DA, Cole BJ. Rehabilitation after autologous chondrocyte implantation in athletes. Clin Sports Med 2010; 29:267-282.
  14. Reinold MM, Wilk KE, Macrina LC, Dugas JR, Cain EL. Current concepts in the rehabilitation following articular cartilage repair procedures in the knee. J Orthop Sports Phys Ther 2006; 36:774-794.
  15. Riegger-Krugh CL, Mccarty EC, Robinson MS, Wegzyn DA. Autologous chondrocyte implantation: current surgery and rehabilitation. Med Sci Sports Exerc 2008; 40:206-214.
  16. Tyler TF, Lung JY. Rehabilitation following osteochondral injury to the knee. Curr Rev Musculoskelet Med 2012. [Epub ahead of print].
  17. Robertson WB, Fick D, Wood DJ, Linklater JM, Zheng MH, Ackland TR. MRI and clinical evaluation of collagen-covered autologous chondrocyte implantation (CACI) at two years. Knee 2007; 14:117-127.
  18. World Health Organization. How to use the ICF: A practical manual for using the Intrernational Classification of Functioning, Disability and Health (ICF). Exposure draft for comment. Geneva: WHO 2013. p.127.
  19. World Health Organization. International Classification of Functioning, Disability and Health. Available from:
  20. Mithoefer K, Mcadams T, Williams RJ, Kreuz PC, Mandelbaum BR. Clinical efficacy of the microfracture technique for articular cartilage repair in the knee: an evidence-based systematic analysis. Am J Sports Med 2009; 37:2053-2063.
  21. Shapiro F, Koide S, Glimcher MJ. Cell origin and differentiation in the repair of full-thickness defects of articular cartilage. J Bone Joint Surg Am 1993; 75:532-553.
  22. Shortkroff S, Barone L, Hsu HP, Wrenn C, Gagne T, Chi T et al. Healing of chondral and osteochondral defects in a canine model: the role of cultured chondrocytes in regeneration of articular cartilage. Biomaterials 1996; 17:147-154.
  23. Stoddart MJ, Ettinger L, Hauselmann HJ. Enhanced matrix synthesis in de novo, scaffold free cartilage-like tissue subjected to compression and shear. Biotechnol Bioeng 2006; 95:1043-1051.
  24. Tew S, Redman S, Kwan A, Walker E, Khan I, Dowthwaite G. Differences in repair responses between immature and mature cartilage. Clin Orthop Relat Res 2001; 391:S142-S152.
  25. Patel VV, Hall K, Ries M, Lotz J, Ozhinsky E, Lindsey C et al. A three-dimensional MRI analysis of knee kinematics. J Orthop Res 2004; 22:283-292.
  26. Mcginty G, Irrgang JJ, Pezzullo D. Biomechanical considerations for rehabilitation of the knee. Clin Biomech 2000; 15:160-166.
  27. Mcconnell J. The physical therapist's approach to patellofemoral disorders. Clin Sports Med 2002; 21:363-387.
  28. Grelsamer RP, Weinstein CH. Applied biomechanics of the patella. Clin Orthop Relat Res 2001; 389:9-14.
  29. Wallace DA, Salem GJ, Salinas R, Powers CM. Patellofemoral joint kinetics while squatting with and without an external load. J Orthop Sports Phys Ther 2002; 32:141-148.
  30. Mithoefer K, Hambly K, Della Villa S, Silvers H, Mandelbaum BR. Return to sports participation after articular cartilage repair in the knee: scientific evidence. Am J Sports Med 2009; 37 Suppl 1:S167-S176.
  31. Lewek MD, Rudolph KS, Snyder-Mackler L. Quadriceps femoris muscle weakness and activation failure in patients with symptomatic knee osteoarthritis. J Orthop Res 2004; 22:110-115.
  32. Van Grinsven S, Van Cingel RE, Holla CJ, van Loon CJ. Evidence-based rehabilitation following anterior cruciate ligament reconstruction. Knee Surg Sports Traumatol Arthrosc 2010; 18:1128-1144.
  33. Ebert JR, Edwards PK. The evolution of progressive postoperative weight bearing after autologous chondrocyte implantation in the tibiofemoral joint. J Sport Rehabil 2014; 23:192-202.
  34. Ebert JR, Ackland TR, Lloyd DG, Wood DJ. Accuracy of partial weight bearing after autologous chondrocyte implantation. Arch Phys Med Rehabil 2008; 89:1528-1534.
  35. Williams JM, Moran M, Thonar EJ, Salter RB. Continuous passive motion stimulates repair of rabbit knee articular cartilage after matrix proteoglycan loss. Clin Orthop Relat Res. 1994 Jul;(304):252-62.
  36. Wondrasch B, Zak L, Welsch GH, Marlovits S. Effect of accelerated weightbearing after matrix-associated autologous chondrocyte implantation on the femoral condyle on radiographic and clinical outcome after 2 years: a prospective, randomized controlled pilot study. Am J Sports Med 2009; 37 Suppl 1:S88-S96.
  37. Fitzgerald GK, Axe MJ, Snyder-Mackler L. Proposed practice guidelines for nonoperative anterior cruciate ligament rehabilitation of physically active individuals. J Orthop Sports Phys Ther 2000; 30:194-203.
  38. Wondrasch B, Aroen A, Rotterud JH, Hoysveen T, Bolstad K, Risberg MA. The feasibility of a 3-month active rehabilitation program for patients with knee full-thickness articular cartilage lesions: the Oslo Cartilage Active Rehabilitation and Education Study. J Orthop Sports Phys Ther 2013; 43:310-324.
  39. Irrgang JJ, Pezzullo D. Rehabilitation following surgical procedures to address articular cartilage lesions in the knee. J Orthop Sports Phys Ther 1998; 28:232-240.
  40. Abt JP, Smoliga JM, Brick MJ, Jolly JT, Lephart SM, Fu FH. Relationship between cycling mechanics and core stability. J Strength Cond Res 2007; 21:1300-1304.
  41. Zazulak BT, Hewett TE, Reeves NP, Goldberg B, Cholewicki J. Deficits in neuromuscular control of the trunk predict knee injury risk: a prospective biomechanical-epidemiologic study. Am J Sports Med 2007; 35:1123-1130.
  42. Zazulak BT, Hewett TE, Reeves NP, Goldberg B, Cholewicki J. The effects of core proprioception on knee injury: a prospective biomechanical-epidemiological study. Am J Sports Med 2007; 35:368-373.


Image by Tayler Pitts

Tags :
Switch Language: list thumbnails
Bookmark and Share


Sports Rehab

Article Images

Copyright © Aspetar Sports Medicine Journal 2022