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815
COMMENTARY
CLINICAL
REVIEW OF LITERATURE
Types of Lesions
Chondral or osteochondral lesions are found in
61% to 66% of knees examined arthroscopically,3,17,37,98 but are less frequently (54%) found in
patients younger than 45 years of age.3 Injury to the
articular cartilage and subchondral bone can induce
early changes of posttraumatic degenerative disease68
and acute subchondral fractures have been shown to
be a factor for future degenerative changes in animal
studies of cartilage, even in the absence of any initial
intra-articular damage.55 Therefore, a geographic
bone bruise is an important variable to include in the
equation for risk of arthritis.43 Chondral and
osteochondral lesions are frequently associated with
other intra-articular disorders.17 The most commonly
noted concomitant injuries are to the anterior cruciate ligament (ACL)3,37,75 and menisci,37,98 as well as
patellar dislocations. 3 During 1000 consecutive
arthroscopies, Hjelle et al37 found focal chondral or
osteochondral lesions in 19% of the knees examined
(excluding chondromalacia), of which 80% were
associated with concomitant ACL or meniscal injury.
Isolated articular lesions do exist, although less frequent. Zamber et al98 noted isolated articular cartilage lesions in 6.2% of 200 knee arthroscopies, and
in a younger population, Thein and Eichenblat93
816
Injury
Response
Consequence
?
Activities
Work
Sport
Joint Injury
Ligament?
Meniscus?
Articular cartilage?
Unknown
factors
Return to
normal
articular
cartilage
function
Genetics
Rehabilitation
Stimulate healing
Protect repair
Prevent further degeneration
Joint Alignment
?
Nutrition
Articular
cartilage
degradation
Sport-Specific Injuries
Sports activities that appear to increase the risk of
OA include those that demand high-intensity, direct
joint impact as a result of contact with other participants, playing surfaces, or equipment.11 Team sports,
such as soccer,23,51 Australian football,20 hockey, and
basketball51 have been linked to a higher risk of knee
disability. Running for fitness and exercise has become a popular activity in the United States. Several
studies have examined distance running and shown
that moderate regular running has low, if any risk of
leading to knee OA.56,69 No significant differences in
incidence of OA have been found between runners
and nonrunners based on radiographic evaluation,56,57 or between long-distance runners and swimJ Orthop Sports Phys Ther Volume 36 Number 10 October 2006
mers.88 Kujala et al54 compared the effects of longterm weight lifting to playing soccer and distance
running. The incidence of knee OA was reportedly
31% in weight lifters, 29% in soccer players, and only
14% in runners. The authors concluded that soccer
players and weight lifters are at increased risk for
developing premature OA, in part explained by a
history of knee injury for soccer players and increased body mass for weight lifters.
Other Considerations
While assessing the patient and planning a rehabilitation program, factors other than type of lesion and
concomitant injuries need to be taken into consideration, such as age, gender, body mass index (BMI),
and time from initial injury. Older patients28,94 and
those who have long-term cruciate ligament deficiencies32,94 are more likely to have more severe cartilage
lesions. This has also been noted for young patients
with a BMI of 25 or greater.28 Zhai et al99 report that
chondral defects, osteophytes, and obesity are the
main determinants of knee pain in younger subjects.
Piasecki et al75 suggest that gender specific differences in lower extremity alignment or injury mechanism could explain why female high school athletes
with ACL injuries sustained fewer injuries to the
medial compartment than males with the same injury.
COMMENTARY
CLINICAL
Repair Process
careful and thorough history and clinical examination of the entire lower extremity. By identifying the
injury mechanism, local contributing factors at the
knee and associated lower extremity contributions, an
accurate differential diagnosis may be established as
well as a carefully planned rehabilitation program.
History
The clinical examination should begin with a
careful and thorough subjective history. A traumatic
origin should be expected, although patients may not
always remember sustaining an injury and some
defects may be the result of repeated minor traumas.37,93 Injuries are often sports or work related and
noncontact in nature.42,93 The history should include
the patients chief complaints, description and location of pain, and the nature of pain patterns (activities that aggravate and alleviate symptoms). Patients
should also report swelling and dysfunction patterns
based on time of day, activities, and the effects their
exercise/sport participation has on their knee joint.
Furthermore, any previous injuries and surgeries of
their knee should be disclosed, as these may place
the individual at a higher risk of developing knee
OA.39,54 The authors recommend obtaining medical
records from previous surgeries and prior treatments.
Lastly, patients should explain their former and
present level of activity, and their functional goals.
Physical Examination
By evaluating lower extremity alignment and function, one may attempt to determine whether the
associated joints are contributing to the dysfunction
at the knee joint. Thus, it is imperative that the
clinical evaluation include not only the knee, but also
the pelvis, hip, foot, and ankle. The presence of genu
varum or genu valgus may lead to greater weightbearing loads and is associated with increased risk of
joint space narrowing in the medial or lateral compartment, respectively.92 In addition, limb length,
femoral anteversion, hip rotation flexibility, pelvis
position, and foot alignment should be carefully
evaluated. Furthermore, alterations in gait can have a
significant effect on the knee joint.
Patients with articular cartilage lesions of the knee
often exhibit joint line pain, swelling and diminished
quadriceps muscle strength. Knee range of motion
(ROM) is often altered, with the patient presenting
with a lack of full knee extension, which may
significantly affect the patients gait mechanics. Limited knee flexion may be due to knee joint swelling
or the development of osteophytes. Soft tissue flexibility, especially the hamstrings and hip flexors, must
also be carefully assessed. Manual muscle testing to
the entire lower extremity helps determine strength
status and presence of pain. Isokinetic testing of the
818
Imaging
The evaluation should include plain radiographs
and possibly an MRI assessment. The plain radiographs should be carefully evaluated for boney abnormalities, osseous spurring, alignment abnormalities,
etc. Risk factors for developing posttraumatic OA
include malalignment, articular cartilage incongruity,
and joint instability.11,12,40 Articular cartilage incongruities greater than 3 mm significantly increase local
contact stresses onto the articular surfaces.9,41 These
articular cartilage incongruities may develop secondary to fractures in the cartilage surfaces. More serious
cartilage injuries are most commonly found at the
medial femoral condyle and the patella.3,17,28,94 An
MRI may be useful to determine meniscus status,
articular cartilage damage, bone bruises, and soft
tissue lesions about the knee joint. Imaging of articular cartilage has been enhanced with the use of
fast-spin-echo MRI that determines the location and
extent of articular cartilage lesions more precisely.77
Treatment Plan
Once the clinical examination is completed, a
thorough and multiphased rehabilitation program
must be outlined. In the opinion of the authors,
compliance to the program is critical to obtaining a
successful outcome. As compliance may be improved
via patient education, the clinician must communicate to the patient information regarding the role of
the rehabilitation program in preservation of articular cartilage. Interventions, such as physical activity,
drugs or dietary factors, are aimed at reducing or
reversing cartilage defects and may reduce the risk of
subsequent knee OA.14
819
COMMENTARY
CLINICAL
should be educated regarding desirable and undesirable activities. We recommend not rushing the patient back to sports that load the affected articular
surfaces excessively when the joint has been injured
or is in a painful episode. The rehabilitation team
should design a rehabilitation program that regulates
and gradually increases the exercise dosage, which
refers to the type and intensity of the exercise, and
the volume (number of repetitions). In the early
stages following articular cartilage injury the exercise
dosage should be low, with gradual increases as the
patient improves. By recognizing the location and
extent of the lesion an accurate and appropriate
rehabilitation program can be developed, with respect to ROM, exercise dosage, joint loading, and
functional activities (Table). For instance, patients
with lesions contained to the patella or trochlea may
be allowed to fully weight bear in a knee immobilizer,
whereas lesions to the weight-bearing area of the
medial femoral condyle may call for initially limiting
a patients weight-bearing status. The location and
extent of articular cartilage lesions can be accurately
determined through fast-spin-echo MRI, as described
by Potter et al.77
TABLE. Exercise examples and progression criteria for rehabilitation of articular lesions in the athletes knee.
TABLE (continued)
Criteria for progressing to next phase
No effusion
Full ROM
Satisfactory muscle strength
No increase in pain or swelling after exercise
Return-to-Activity Phase (Sport-Specific Activities)
Strength and flexibility
Continue stretches before and after exercise program
Continue progressing strength
Functional activities
Running
- Progress type of running (cutting, agility)
- Progress intensity and duration of runs
Jumping
Sport-specific movements and drills
Gradual return to sport at preinjury levels
COMMENTARY
CLINICAL
* Denotes exercises or advice where special consideration must be given to the patellofemoral joint and may not be applicable.
the abdominal region and trunk stabilization exercises may continue to be implemented during this
phase.
COMMENTARY
CLINICAL
SUMMARY
The nonoperative treatment of articular cartilage
lesions of the knee joint is a common and challenging task for the medical team. Knee articular cartilage
lesions are especially challenging in the patient who
desires an active athletic lifestyle. Athletes who have
injured their knee appear to be more susceptible in
developing tibiofemoral joint articular cartilage lesions and later OA, especially if the injury included
the meniscus or ACL, or a bone bruise was present.
Other factors that increase the risk of developing OA
include malalignment, joint deformity, articular cartilage incongruities, high BMI, age, gender, quadriceps
weakness, and nutrition. The rehabilitation specialist
should recognize these risk factors and treat the
patient appropriately. Bone bruises should be considered a serious injury and may progress to articular
cartilage full-thickness lesions. The rehabilitation specialist should manage the patient with a multiphased
approach, using sound mechanical principles and the
available scientific evidence. During each phase of
the rehabilitation program, specific goals must be
determined and specific criteria accomplished prior
to the progression to the next phase. The ultimate
goal of the rehabilitation program is the long-term
functional level of the patient. By approaching the
patient with these treatment guidelines, the authors
believe it will ensure the long-term optimal function
of the knee joint.
REFERENCES
1. Ahmed AM, Burke DL. In-vitro measurement of static
pressure distribution in synovial joints--Part I: Tibial
surface of the knee. J Biomech Eng. 1983;105:216-225.
2. Ahmed AM, Burke DL, Yu A. In-vitro measurement of
static pressure distribution in synovial joints--Part II:
Retropatellar surface. J Biomech Eng. 1983;105:226236.
3. Aroen A, Loken S, Heir S, et al. Articular cartilage
lesions in 993 consecutive knee arthroscopies. Am J
Sports Med. 2004;32:211-215.
4. Bassleer C, Henrotin Y, Franchimont P. In-vitro evaluation of drugs proposed as chondroprotective agents. Int
J Tissue React. 1992;14:231-241.
5. Bassleer CT, Combal JP, Bougaret S, Malaise M. Effects
of chondroitin sulfate and interleukin-1 beta on human
articular chondrocytes cultivated in clusters.
Osteoarthritis Cartilage. 1998;6:196-204.
6. Bellamy N, Campbell J, Robinson V, Gee T, Bourne R,
Wells G. Viscosupplementation for the treatment of
osteoarthritis of the knee. Cochrane Database Syst Rev.
2005;CD005321.
7. Brandt KD, Heilman DK, Slemenda C, et al. A comparison of lower extremity muscle strength, obesity, and
depression scores in elderly subjects with knee pain
with and without radiographic evidence of knee
osteoarthritis. J Rheumatol. 2000;27:1937-1946.
8. Brandt KD, Heilman DK, Slemenda C, et al. Quadriceps
strength in women with radiographically progressive
J Orthop Sports Phys Ther Volume 36 Number 10 October 2006
9.
10.
11.
12.
13.
14.
17.
18.
19.
20.
21.
22.
23.
24.
25.
26.
28.
29.
30.
31.
32.
33.
34.
35.
36.
37.
38.
39.
40.
41.
42.
43.
44.
45.
825
COMMENTARY
16.
27.
injury or reconstruction of the anterior cruciate ligament. Instr Course Lect. 1999;48:185-198.
Ericson MO, Nisell R. Tibiofemoral joint forces during
ergometer cycling. Am J Sports Med. 1986;14:285-290.
Eskelinen AP, Visuri T, Larni HM, Ritsila V. Primary
cartilage lesions of the knee joint in young male adults.
Overweight as a predisposing factor. An arthroscopic
study. Scand J Surg. 2004;93:229-233.
Felson DT, Anderson JJ, Naimark A, Walker AM,
Meenan RF. Obesity and knee osteoarthritis. The
Framingham Study. Ann Intern Med. 1988;109:18-24.
Fowler PJ. Bone injuries associated with anterior cruciate ligament disruption. Arthroscopy. 1994;10:453-460.
Fukubayashi T, Torzilli PA, Sherman MF, Warren RF. An
in vitro biomechanical evaluation of anterior-posterior
motion of the knee. Tibial displacement, rotation, and
torque. J Bone Joint Surg Am. 1982;64:258-264.
Geissler WB, Whipple TL. Intraarticular abnormalities in
association with posterior cruciate ligament injuries. Am
J Sports Med. 1993;21:846-849.
Goldberg VM, Buckwalter JA. Hyaluronans in the
treatment of osteoarthritis of the knee: evidence for
disease-modifying activity. Osteoarthritis Cartilage.
2005;13:216-224.
Graf BK, Cook DA, De Smet AA, Keene JS. Bone
bruises on magnetic resonance imaging evaluation of
anterior cruciate ligament injuries. Am J Sports Med.
1993;21:220-223.
Harrison RA, Bulstrode SJ. Percentage of weight-bearing
during partial immersion in the hydrotherapy pool.
Physiotherapy. 1987;3:60-63.
Hewett TE, Noyes FR, Barber-Westin SD, Heckmann TP.
Decrease in knee joint pain and increase in function in
patients with medial compartment arthrosis: a prospective analysis of valgus bracing. Orthopedics.
1998;21:131-138.
Hjelle K, Solheim E, Strand T, Muri R, Brittberg M.
Articular cartilage defects in 1,000 knee arthroscopies.
Arthroscopy. 2002;18:730-734.
Ho SS, Illgen RL, Meyer RW, Torok PJ, Cooper MD,
Reider B. Comparison of various icing times in decreasing bone metabolism and blood flow in the knee. Am J
Sports Med. 1995;23:74-76.
Hoffman DF. Arthritis and exercise. Prim Care.
1993;20:895-910.
Honkonen SE. Degenerative arthritis after tibial plateau
fractures. J Orthop Trauma. 1995;9:273-277.
Huber-Betzer H, Brown TD, Mattheck C. Some effects
of global joint morphology on local stress aberrations
near imprecisely reduced intra-articular fractures.
J Biomech. 1990;23:811-822.
Huegli RW, Moelleken SM, Stork A, et al. MR imaging
of post-traumatic articular cartilage injuries confined to
the femoral trochlea. Arthroscopic correlation and clinical significance. Eur J Radiol. 2005;53:90-95.
Johnson DL, Bealle DP, Brand JC, Nyland J, Caborn
DNM. The effect of a geographic lateral bone bruise on
knee inflammation after acute anterior cruciate ligament
rupture. Am J Sports Med. 2000;28:152-155.
Johnson DL, William PU, Caborn DNM, Vanarthos WJ,
Carlson CS. Articular cartilage changes seen with magnetic resonance imaging-detected bone bruises associated with acute anterior cruciate ligament rupture. Am J
Sports Med. 1998;26:409-414.
Jorgensen U, Sonne-Holm S, Lauridsen F, Rosenklint A.
Long-term follow-up of meniscectomy in athletes. A
prospective longitudinal study. J Bone Joint Surg Br.
1987;69:80-83.
CLINICAL
15.
osteoarthritis of the knee and those with stable radiographic changes. J Rheumatol. 1999;26:2431-2437.
Brown TD, Anderson DD, Nepola JV, Singerman RJ,
Pedersen DR, Brand RA. Contact stress aberrations
following imprecise reduction of simple tibial plateau
fractures. J Orthop Res. 1988;6:851-862.
Bruyere O, Honore A, Ethgen O, et al. Correlation
between radiographic severity of knee osteoarthritis and
future disease progression. Results from a 3-year prospective, placebo-controlled study evaluating the effect
of glucosamine sulfate. Osteoarthritis Cartilage.
2003;11:1-5.
Buckwalter JA, Lane NE. Athletics and osteoarthritis.
Am J Sports Med. 1997;25:873-881.
Buckwalter JA, Mankin HJ. Articular cartilage: degeneration and osteoarthritis, repair, regeneration, and
transplantation. J Bone Joint Surg. 1997;79A:612-632.
Childs JD, Sparto PJ, Fitzgerald GK, Bizzini M, Irrgang
JJ. Alterations in lower extremity movement and muscle
activation patterns in individuals with knee
osteoarthritis. Clin Biomech (Bristol, Avon). 2004;19:4449.
Cicuttini F, Ding C, Wluka A, Davis S, Ebeling PR,
Jones G. Association of cartilage defects with loss of
knee cartilage in healthy, middle-age adults: a prospective study. Arthritis Rheum. 2005;52:2033-2039.
Cox JS, Cordell LD. The degenerative effects of medial
meniscus tears in dogs knees. Clin Orthop Relat Res.
1977;236-242.
Crenshaw SJ, Pollo FE, Calton EF. Effects of lateralwedged insoles on kinetics at the knee. Clin Orthop
Relat Res. 2000;185-192.
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.
Daniel DM, Stone ML, Dobson BE, Fithian DC, Rossman DJ, Kaufman KR. Fate of the ACL-injured patient.
A prospective outcome study. Am J Sports Med.
1995;23:372-373.
Das A, Jr., Hammad TA. Efficacy of a combination of
FCHG49 glucosamine hydrochloride, TRH122 low molecular weight sodium chondroitin sulfate and manganese ascorbate in the management of knee
osteoarthritis. Osteoarthritis Cartilage. 2000;8:343-350.
Deacon A, Bennell K, Kiss ZS, Crossley K, Brukner P.
Osteoarthritis of the knee in retired, elite Australian
Rules footballers. Med J Aust. 1997;166:187-190.
Ding C, Cicuttini F, Scott F, Boon C, Jones G. Association of prevalent and incident knee cartilage defects
with loss of tibial and patellar cartilage: a longitudinal
study. Arthritis Rheum. 2005;52:3918-3927.
Dodge GR, Jimenez SA. Glucosamine sulfate modulates
the levels of aggrecan and matrix metalloproteinase-3
synthesized by cultured human osteoarthritis articular
chondrocytes. Osteoarthritis Cartilage. 2003;11:424432.
Drawer S, Fuller CW. Perceptions of retired professional
soccer players about the provision of support services
before and after retirement. Br J Sports Med.
2002;36:33-38.
Drovanti A, Bignamini AA, Rovati AL. Therapeutic
activity of oral glucosamine sulfate in osteoarthrosis: a
placebo-controlled double-blind investigation. Clin
Ther. 1980;3:260-272.
Dye SF, Chew MH. Restoration of osseous homeostasis
after anterior cruciate ligament tear. Am J Sports Med.
1993;21:748-750.
Dye SF, Wojtys EM, Fu FH, Fithian DC, Gillquist I.
Factors contributing to function of the knee joint after
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96.
97.
98.
99.
COMMENTARY
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CLINICAL
827
1. Barbara Wondrasch, Asbjrn ren, Jan Harald Rtterud, Turid Hysveen, Kristin Blstad, May Arna Risberg. 2013. 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. Journal of Orthopaedic & Sports Physical Therapy 43:5, 310-324. [Abstract] [Full Text] [PDF] [PDF
Plus]