Chapter 11: Articular Cartilage Lesions in Patellofemoral Pain Patients


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    Figure 11.1. The specific pattern of patellofemoral alignment will determine the nature, location, and extent of cartilage breakdown.

    Figure 11.2. Operative photo of closed chondromalacia. The reflection of light is off a rounded "blister" lesion, which projects above the surface. Arrow marks proximal border at median ridge; lateral facet superior.

    Figure 11.3. A, Cross‑section of a patella removed at autopsy through the 40‑degree flexion zone shows deep fiissured cartilage localized to the critical zone with fissures extending to the subchondral bone. B, Arthroscopic view of a critical zone lesion similar to that noted in 11.3, A.

    Figure 11.4. Patellar articular cartilage fibrillation less than ½ inch in diameter (Outerbridge Grade 2 changes) as viewed with an arthroscope. Photo courtesy of Dandy D. Arthroscopy of the Knee slide collection, Gower Medical Publishing.

    Figure 11.5. Patellar articular cartilage fibrillation greater than 1/2 inch in diameter (Outerbridge Grade 3 changes) as viewed with an arthroscope. Photo courtesy of Dandy D. Arthroscopy of the Knee slide collection, Gower Medical Publishing.

    Figure 11.6. A, Arthroscopic view of extensive patella articular cartilage loss with (B) erosion to bone. C, Medial condyle erosion related to medial meniscus damage can cause reciprocal changes on the patella.

    Figure 11.7. This patient sustained a proximal pole crush, which resulted in full‑thickness (Grade 4) articular cartilage loss to bone when viewed with an arthroscope.

    Figure 11.8. Overzealous medial imbrication, medial tubercle transfer, or posteromedial tibial tubercle transfer (Hauser) can cause erosion of distal medial patella cartilage to bone. This patient needed anterolateral transfer of the tibial tubercle.

    Figure 1 1.9. A, A representation of the normal patella (medial left; lateral right). B, A Type I lesion (Ficat critical zone) at the distal central ridge. C, A Type II lesion of the lateral facet is usually related to excessive lateral pressure with tilt. This lesion is often associated with a Type I lesion, and the two lesions may connect, particularly in a patient with longstanding lateral patellar tilt and subluxation. D, A Type III lesion will occur related to relocation of a patella following dislocation, with shearing off of the medial facet. Lesions of the medial facet also occur from excessive medial overload (overzealous medial imbrication or Hauser transfer of the tibial tubercle). E, The proximal patellar lesion (Type IV) that spans the facets is most often related to a crush, knee flexion injury (dashboard type) in which the proximal patella is articulating (knee flexed) at the time of impact. F, End‑stage diffuse patella articular cartilage degeneration. Illustrations by Phoebe Fulkerson.

    Figure 11. 10. Transmission electron micrograph of a Stage I lesion; superficial layer showing the surface to be intact.

    Figure 11.11. Chondrocyte from intermediate zone (C2) showing increased pinocytosis. FF = fine filaments.

    Figure 11.12. Chondrocyte from superficial layer at the median ridge. Abundance of fine filaments (FF)and cytoplasmic villi abound.

    Figure 11.13. Deep portion superficial layer, median ridge, Stage I lesion. Abundant glycogen (G), well‑de­veloped Golgi apparatus (arrows).

    Figure 11.14. Superficial C2 layer. The cell is surrounded by a ring of proteoglycans (PG) and an amorphous microfibrillar ring (arrows).

    Figure 11.15. Deeper in layer C2. Cellular multiplication and cloning is evident.

    Figure 11.16. Median ridge, C1 layer. Metabolically active cell dense bodies (DB).

    Figure 11.17. Layer C2 at median ridge, closed chondromalacia. Marked dilatation of the endoplasmic reticulum (arrows).

    Figure 11.18. Superficial layer, lateral facet. Mitochondria without cristae (M)‑some with rupture (arrows).

    Figure 11.19. Superficial layer at the "critical zone" showing markedly irregular fiber direction.

    Figure 11.20. Marked variation in fiber diameter from 100 to 500 angstroms. There is also considerable sep­aration of fibers for this layer.

    Figure 11.21. Superficial layer, medial facet. Fibers are disorganized, disoriented, and separated by abundant ground substance. Tremendous variation in fiber thickness from 220 to 1100 angstroms.

    Figure 11.22. Superficial layer. Fiber fragmentation and dissociation by edema.

    Figure 11.23. Superficial layer, medial facet. Fiber disintegration.

    Figure 11.24. Lateral facet, superficial layer. Marked fiber separation by edema.

    Figure 11.25. C2 layer. Fissures are evident, which may be artifactual but only seem to occur in advanced cases.

    Figure 11.26. Deep portion, superficial layer. Fissure lined by electron‑dense material is certainly not artifactual.

    Figure 11.27. Superficial portion of C2; fissure with a randomly oriented fibrillar border.

    Figure 11.28. Zone C2. Disappearance of organelles.

    Figure 11.29. Chondrocyte from zone C2 showing homogenization of a portion of the cytoplasm and di­latation of the endoplasmic reticulum (ER).

    Figure 11.30. Superficial layer, medial facet in Stage II lesion showing a more or less extensive degeneration of the cytoplasmic membrane (intact membrane seen at arrows).

    Figure 11.31. Deep layer in an advanced cartilage lesion showing rupture and fragmentation of the cyto­plasm.

    Figure 11.32. Chondrocyte of the superficial layer showing alteration of chromatin patterns.

    Figure 11.33. Chondrocyte from zone C1. Thickened and greatly invaginated nuclear membrane.

    Figure 11.34. Zone C3. This could represent several nuclei undergoing fragmentation and rupture. N = nuclear fragment.

    Figure 11.35. A, View of the articular surface of a patella removed for permanent lateral subluxation. Note the preservation of a superior and medial cartilage. The patient had only 80 degrees of flexion. B, Tangential view through the midportion of the patella.

    Figure 11.36. Zone C1 in a patient with chondrosclerosis.

    Figure 11.37. Superficial layer, middle portion. Contrast the compactness of the fibers in this condition to Figure 11.20.

    Figure 11.38. Same patient as in Figure 11.37. Deep in zone C2.

    Figure 11.39. Superficial aspect, zone C2. FF = fine filaments.

    Figure 11.40. Zone C2. Chondrosclerosis (dense black globules—arrows).

    Figure 11.41. Zone C1. Glycogen in abundance (G).

    Figure 11.42. Same patient as in Figure 11.41, zone C2. Proteoglycan (PG) crown limited by a microfibrillar layer (arrows).

    Figure 11.43. Deep C2 layer. Multiple cell groupings.

    Figure 11.44. Chronic patellar tilt with subluxation will eventually lead to lateral facet breakdown.

    Figure 11.45. The lateral trochlea of this 16‑year‑old girl with recurrent patellar dislocation shows ample evidence of chronic injury.
    Figure 11.46. A, Massive osteophytosis had nearly doubled the patellar height and extended the trochlear margins proximally. B, Medial and lateral osteophytes have created a secondary patella magna.

    Figure 11.47. A, Standing anteroposterior (AP) view‑the knee shows moderate valgus with lateral joint line narrowing. B, Axial view shows significant lateral patellofemoral arthrosis.

    Figure 11.48. The combination of medial joint line narrowing on the standing AP radiograph of the knee (A) and significant lateral patellofemoral arthrosis (B) is quite common. It is important that the patellofemoral joint be radiologically evaluated when tibiofemoral arthrosis is suspected.

    Figure 11.49. Medial patellofemoral arthrosis with joint line irregularity, osteophytes, and subchondral thickening.

    Figure 11.50. CT reveals early lateral facet collapse secondary to chronic tilt.

    Figure 11.51. As the lateral facet collapses, osteophytes form along the trochlea, and there may be some evidence of increasing tilt or subluxation.

    Figure 11.52. Trochlear osteophytes, (A‑C) either from (A) the degenerative process or from (B) trauma, can cause mechanical symptoms and pain that may warrant debridement.

    Figure 11.52. Continued.


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