Management of chondromalacia patellae in elite athletes: Balancing high-performance demands with joint preservation

Static malalignment

A larger Q angle (often >20° in women, >15° in men) increases the lateral pull on the patella, a classic risk factor for lateral facet overload and (CP). On the one hand, the valgus malalignment increases the Q-angle, which in turn increases the stress on the lateral PFJ. On the other hand, varus malalignment at the knees leads to medial PFJ overload, which can cause cartilage degeneration.

Dynamic malalignment (more significant than static)

Weak hip abductors/external rotators (gluteus medius) lead to excessive femoral internal rotation during weight-bearing, causing a “functional” valgus and lateral patellar tracking. Excessive pronation of the foot causes internal tibial rotation, twisting the patellar tendon attachment and increasing lateral patellar tilt.

Rotational malalignment

Excessive femoral anteversion and tibial extorsion create a “miserable malalignment syndrome,” causing rotational mismatch and severe patellar maltracking.

Weight-bearing anteroposterior and lateral views

X-rays are used to detect other conditions that may cause anterior knee pain and to evaluate the PFJ. This helps assess overall alignment, trochlear morphology, patellar alta (InsallSalvati ratio >1.2, Caton-Deschamps ratio >1.3), and signs of osteoarthritis. Furthermore, it helps to rule out fractures, osteoarthritis, osteochondral defects, loose bodies, tumors, or significant joint space narrowing.

Axial (merchant/sunrise) view at 30–45° of flexion

This view is essential for evaluating PF congruence, lateral patellar tilt, and subluxation. It can show joint space narrowing and osteophyte formation, but does not visualize cartilage directly. An increased sulcus angle with a positive congruence angle is a risk factor for patellar instability. Furthermore, the lateral patellar displacement ratio is <0.05–0.10. Ratios >0.20 are strongly associated with patellar instability and a history of dislocation.

Fat-suppressed proton density or T2-weighted fast spin-echo sequences

These are the primary sequences for morphological assessment. Fat suppression is critical for detecting concomitant bone marrow edema, a significant source of pain. They provide excellent detail of cartilage surface integrity and underlying bone.

Three-dimensional (3D) gradient-echo sequences

These include spoiled gradient recalled or dual echo in steady state sequences. These allow for thin, contiguous slices (<1.5 mm) and are excellent for volumetric assessment and detecting subtle surface irregularities.^[11]

Intermediate-weighted fat-suppressed sequences

These sequences offer an optimal balance between T1 and T2 weighting, providing high contrast between bright synovial fluid and intermediate-signal cartilage, making fissures and defects more conspicuous.

T2 mapping

This sequence helps quantify collagen matrix integrity and hydration. Early chondromalacia often shows elevated T2 values due to increased water content and collagen disorganization before morphological changes are visible.

T1rho mapping

This sequence is highly sensitive to loss of proteoglycan content in the cartilage extracellular matrix, another early biochemical marker of degeneration.

Delayed gadolinium-enhanced MRI of cartilage

This sequence assesses glycosaminoglycan (GAG) concentration by measuring T1 relaxation time after intravenous gadolinium administration. Lower GAG correlates with early degeneration.

MRI findings include cartilage changes, which are graded according to outerbridge or International Cartilage Repair Society (ICRS) classification systems [Tables 1 and 2].^[12] Additional changes include bone marrow edema in the patella or trochlea (“kissing lesions”), synovitis, effusion, trochlear dysplasia, and lateral patellar tilt.

Load management

In this phase, the athletes are offered “relative rest.” This involves reducing impact and high-flexion activities (squats, stairs) by 50–70%. The athletes utilize cross-training (pool running, anti-gravity treadmills) to maintain cardiopulmonary fitness without exacerbating pain (Visual Analog Scale [VAS] <3/10).

Pain and inflammation management

This is achieved by a short course of non-steroidal anti-inflammatory drugs and cryotherapy. Further analgesics like opioids may be administered based on the requirement. Control of pain and inflammation is essential for early rehab.

Early rehabilitation

Initially, the isometric exercises are encouraged. Isometric quadriceps exercises (straight leg raises, quad sets) at multiple angles, with vastus medialis obliquus (VMO) strengthening, must be performed along with hip and ankle strengthening.

Strength and neuromuscular control

Gradual progression to eccentric exercises (e.g., decline single-leg squats, Nordic hamstring curls for the posterior chain) is carried out after 2 weeks. This increases the tendon and cartilage tolerance.^[16] The proximal muscles, like gluteus medius/maximus, are strengthened during this period to control femoral internal rotation/adduction and reduce dynamic valgus. Further VMO strengthening is done to reduce the stress on the lateral patellar facet.

Load reintegration

A stepwise, symptom-guided progression from low-impact bilateral to high-impact unilateral activities is then followed. During this phase, the trainers must ensure that the pain activity is controlled (Target VAS <5) and subsides within 24 h of activity cessation. Although this pain control model has been applied to Achilles tendinopathy, it also holds good for knee injuries.^[17]

Adjunctive treatment

This includes bracing and taping. Medial glide or McConnell taping for the patella can be used for symptomatic relief during sport-specific training. PF braces with a lateral buttress may be considered for athletes with maltracking. One may consider foot orthoses, such as arch-support insoles and deep heel cups, if significant biomechanical foot issues, such as excessive pronation, are noted.

Platelet-rich plasma (PRP)

PRP shows promise for symptomatic improvement and potential cartilage modulation in early-stage chondromalacia (Outerbridge I-II).^[18] However, evidence for altering structural progression in athletes remains limited. If used at all, a leukocyte-deficient PRP must be administered. An initial inflammatory response may be expected after the injection, which subsides with time. This inflammatory phase must be managed with rest and ice pack applications.

Bone marrow aspirate concentrate

It contains mesenchymal stem cells (MSCs) and growth factors. Emerging as a potential option for focal, contained Grade III–IV lesions in athletes wishing to delay or avoid surgery, though high-level evidence is still evolving. Furthermore, the high cost of treatment limits its use in clinical practice. An inflammatory reaction may occur after injection, similar to that seen with PRP.

Viscosupplementation

Although strictly not an orthobiologic, these agents can be used for the treatment of chondromalacia. These agents also reduce inflammation and enhance patellar gliding. Only a handful of studies have been conducted on patients with chondromalacia, but the results are pretty encouraging.^[19,20]

MSCs

Injecting pluripotent MSCs derived from adipose tissues has proven to be beneficial in the management of CMP. The adipocytes are retrieved from the patient through liposuction and treated to generate the MSCs.^[21] The MSC suspension is then injected into the knee. The MSCs get activated into chondrocytes by transforming growth factor-beta, which replaces the cells.^[22] The MSCs also help control the inflammatory milieu and contribute to healing.

Microfracture

This technique is also used for small lesions. The degenerated cartilage is debrided, and a punch is used to remove the degenerated part. An osteochondral plug is extracted from the lesser articulating portion of the superolateral trochlear groove with the help of a punch or reamers. This plug is then placed on the debrided cartilage.^[23-25] This is usually performed by medial arthrotomy. For larger lesions, multiple osteochondral plugs can be harvested and implanted. A recent review by Donoso et al. found that osteochondral autograft transplantation (OAT) is a highly efficient way of treating high-grade patellar chondral lesions.^[26]

OATs/mosaicoplasty

This technique is also used for small lesions. The degenerated cartilage is debrided, and a punch is used to remove the degenerated part. An osteochondral plug is extracted from the lesser articulating portion of the superolateral trochlear groove with the help of a punch or reamers. This plug is then placed on the debrided cartilage.^[25] This is usually performed by medial arthrotomy. For larger lesions, multiple osteochondral plugs can be harvested and implanted. A recent review by Donoso et al. found that OATs are a highly efficient way of treating high-grade patellar chondral lesions.^[26]

PF allografts

Recently, authors have tried using PF allografts and have demonstrated success. The osteochondral allograft completely integrates with the host bone.^[27] These can be used in skeletally immature patients at risk of physeal injury during harvesting of the femoral autograft. However, there are no randomized controlled trials (RCTs) involving the use of an allograft.

Matrix-induced autologous chondrocyte implantation (MACI)

Chondrocyte implantation (CI) restores the hyaline cartilage as opposed to fibrocartilage obtained after microfracture. It is a two-stage procedure: The first stage involves harvesting chondrocytes, either arthroscopically or through an open procedure, followed by in vitro culture and cell expansion. In the second stage, these cells are then replanted into the cartilage defect [Figure 3]. Autologous chondrocyte implantation (ACI) may be considered in larger full-thickness chondral defects (>2 cm²) on the patella or trochlea. However, this procedure requires prolonged RTS (9–12+ months) but offers hyaline-like repair. This technique certainly has favorable outcomes as compared to the previously mentioned techniques.^[28]

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Figure 3:

Autologous chondrocyte implantation for chondromalacia patella. (A and B) The lesion present on the lateral facet of petalla was debrided. (C and D) Then, cultured chondrocytes mixed with thrombin and fibrin were put to the defect site.

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MPFL reconstruction

Since the MPFL is the primary restraint to lateral patella subluxation from 0° to 30° of flexion, this procedure is the gold standard for recurrent patella instability. It involves anatomic and isometric reconstruction of the MPFL. A semitendinosus or a gracilis autograft replaces the incompetent MPFL.

The graft is secured at Schottle’s point on the femoral side, which lies 1 mm anterior to the tangent to the posterior femoral cortex, 2.5 mm distal to the perpendicular line traced through the initial part of the medial femoral condyle, and proximal to the vertical line traced through the most posterior part of Blumensaat’s line. Care must be taken not to damage the physis in case of skeletally immature athletes. In such cases, the semitendinosus autograft can be suspended around the adductor longus tendon instead of drilling the femoral bone. The patellar attachment lies at 7.4 ± 3.5 mm anterior to the posterior patellar cortical line, 5.4 ± 2.6 mm distal to the perpendicular line intersecting the proximal margin of the patellar articular surface.^[29]

The complications of this procedure range from 0% to 32.3%.^[30] The most common complication is the stiffness of the knee (20%), followed by failure of the graft (10.7%) and patella fractures (8.3%).^[30] The prevalence of persistent anterior knee discomfort has been reported to range from 0% to 32.3% in patients. Hence, early physiotherapy is indicated after surgery.

Tibial tubercle osteotomy (TTO)

This surgery is performed in cases of high-riding patella. The tibial tubercle is osteotomized with an oscillating saw. The osteotomized tubercle should be at least 2 cm in breadth and 8–10 cm in length. The osteotomized tubercle is then released from its soft-tissue attachments. It is then anteriorized, distalized, or medialized depending on the requirement and fixed using plates or screws.^[31-33] TTO has the following variants based on the direction of movement of the tibial tubercle. This surgery is performed in cases of high-riding patella. The tibial tubercle is osteotomized with an oscillating saw. The osteotomized tubercle should be at least 2 cm in breadth and 8–10 cm in length. The osteotomized tubercle is then released from its soft-tissue attachments. It is then anteriorized, distalized, or medialized depending on the requirement and fixed using plates or screws.^[31] TTO has 3 variants based on the direction of tibial tubercle movement.

Anteriorization (Maquet)

Anteriorization of the tibial tubercle is achieved by placing a bone graft below the tibial tubercle. This reduces the patella-femoral contact forces. Maquet revealed that a 2 cm anteriorization reduced PF contact forces by 50%.^[32] It is helpful in the management of combined chondrosis and instability.^[32] However, this technique carries a complication rate of 10–30%, mostly leading to skin necrosis and prominence of hardware, compartment syndrome, and non-union.^[33] Hence, this technique is not popular nowadays.

Medialization (Elmslie-Trillat)

The primary indication for this surgical technique is patellar instability or lateral maltracking. Medialization of the tibial tubercle reduces the lateral maltracking. If done correctly, it reduces the recurrence rates to <7%.^[34]

Anteromedialization (Fulkerson/Antero-Mediali-Zation [AMZ])

The procedure of choice for athletes with instability and significant lateral facet overload/chondrosis. This is a combination of the methods mentioned above. Initially described by Fullkerson et al. in 1983, this technique is the main workhorse in the management of PFPS today. The indications include PF pain not responding to non-operative interventions and patellar maltracking (including instability) or excessive tilt.^[35] Lateral and distal chondral wear is the usual pattern of wear associated with lateral maltracking of the patella. In addition to allowing the patella to make contact with the trochlea earlier in flexion and shifting the contact area off of the distal patella and more proximally, anteromedialization of the tibial tubercle aids in realigning the extensor mechanism and improving patellar tracking.^[36] This technique also carries the risk of skin necrosis, fracture of the osteotomized segment, and non-union of the osteotomy. Complications can be reduced by meticulous soft-tissue dissection, minimal periosteal stripping, and preservation of the blood supply to the osteotomized fragment.^[37]

Medial closing wedge patellar osteotomy

This technique creates a congruent PFJ by altering the shape of the trochlea. Often combined with trochleoplasty, this technique improves the PF maltracking and reduces the abnormal contact forces. A V-shaped wedge of bone is removed from the medial patellar facet, making it congruent to the trochlea.^[38] However, this is technically demanding, and fracture and avascular necrosis of the patella have been reported.

Trochleoplasty

Trochleoplasty is a surgical option in patients with patella instability with severe trochlear dysplasia (Dejour C and B). It involves subchondral deepening and wedge osteotomy of the distal femur. Various types of trochleoplasty have been described, which include:^[39,40]

1. Lateral facet elevation trochleoplasty: This type of trochleoplasty deepens the trochlear groove by augmenting the lateral femoral condyle.

2. Bereiter’s Sulcus deepening trochleoplasty: This is a classic trochleoplasty, which involves deepening the sulcus.

3. Recession wedge trochleoplasty: This type of trochleoplasty addresses the prominent supratrochlear spur and prevents the patella from overriding it and becoming unstable during knee flexion.

De-rotational distal femur osteotomy

The rotational deformity of the femur is often overlooked by surgeons while treating a patella-femoral pathology. An increased femoral anteversion of more than 20° predisposes to recurrent PF dislocations and subluxations.^[41] This can be addressed with a distal metaphyseal de-rotation osteotomy, which can be fixed with plates or an intramedullary device.^[42] However, this technique requires a good number of skills and proper training. This procedure also carries the risk of fat/air embolism, pulmonary embolism, hypotension, oxygen desaturation, and higher mortality. This can be overcome by predrilling the osteotomy and limiting reaming into the canal.^[43]

Soft tissue balancing

Lateral retinaculum release and medial plication can be performed as an adjunct to bony procedures.

Subchondroplasty

This is a novel technique used to address the subchondral insufficiency fractures (bone marrow edema on MRI) associated with cartilaginous softening. This involves percutaneous injection of calcium phosphate into the subchondral bone to stabilize the articular surface under the guidance of fluoroscopy^[46] [Figure 4].

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Figure 4:

Subchondroplasty technique.

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Nanofracture and autologous matrix-induced chondrogenesis (AMIC)

Nanofracture involves the use of more precise needles (1 mm diameter and 9 mm deep) for bleeding the subchondral bone. This technique works on the principle of microfracture. However, the outcomes of nanofracture alone are poor, as MSCs are washed out of the nanofracture site by synovial fluid. The addition of a hyaluronic acid-based scaffold holds the MSCs at the microfracture site and enhances the quality of fibrocartilage formed.^[47] This technique is known as AMIC [Figure 5]. This can also be done arthroscopically. Behrendt et al. reported great clinical outcomes with AMIC; however, RCTs are awaited.^[48]

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Figure 5:

Autologous matrix-induced chondrogenesis.

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