The History

In order for a surgeon to have a successful relationship with a patient, the desires, needs, and expectations of the patient must be balanced with what is possible. The surgeon must use his or her best judgment and draw upon the best available evidence and his or her own experience and skills to match these goals. If this is not possible, then the patient should be referred to an expert on the condition. Patients often present with pain and limitation of function. They are often anxious and have different reasons for the appointment. Determining the pathology and considering surgical options may not necessarily be the patient’s goal.

An opening questions such as “What is your goal in coming to see me today?” usually helps to direct the surgeon’s line of questioning and the treatment options offered to the patient. The patient may respond as follows:

Alternatively, the patient may be self-referred based on his or her own ambitions. This is becoming more commonplace in the modern age of the Internet because patients are often well informed and wish to take matters into their own hands (“empowerment of the patient”). Figure 4–1 illustrates this concept. A useful tool for developing a healthy relationship with the patient is the five Es (Figure 4–2).

Figure 4–1 Empowerment of the patient.

Figure 4–2 The five Es is a useful tool for developing a healthy relationship with the patient.

Cartilage repair and joint preservation are relatively new topics in the orthopedic management of young patients, as no large cohorts of patients have received treatment or been followed for the long term. Information obtained from the Internet is not always reliable, is not peer reviewed, and may be market driven; therefore, it is up to the orthopedic surgeon to know the existing evidence and to present it to the patient as an educator, patient advocate, and doctor.

Patient Characteristics

The surgeon’s recommendation of treatment options may well depend on patient characteristics. A patient who has a high sense of vitality and an optimistic outlook with strong social supports has demonstrated a good clinical outcome with almost any surgical procedure. We reviewed our clinical outcome data using the Medical Outcomes Study 36-Item Health Survey (SF-36)¹ and noted that vitality and social supports played strong into a positive clinical outcome with regard to physical pain relief and well-being (presented at the International Cartilage Repair Society 2002). I have also found that patients who are athletic at baseline and had a relatively acute injury less than 1 year do better clinically after surgery.^2–4 It is suspected that as the athlete becomes deconditioned, the injury becomes chronic, with thickened subchondral bone and expanding margins such that both the patient and the lesion require more extensive rehabilitation. Obesity is another factor that surgeons encounter. It is approaching epidemic proportions in the United States, with approximately 30% of the population being considered obese. The osteotomy literature had demonstrated that body weight greater than 1.32 times normal adversely affects the outcome and survivorship of osteotomy surgery.⁵ Obesity has also been shown to correlate with an increased incidence of osteoarthritis, which presumably corresponds to enlargement of an existing cartilage defect, or factors adversely toward a cartilage repair procedure because of the force across the regenerative tissue. Counseling the patient regarding weight loss prior to a biologic repair procedure may actually prevent the need for the procedure based on symptom relief with weight loss. For the morbidly obese with body mass index (BMI) greater than 40, surgical gastric bypass surgery may be necessary. Some insurance carriers in the United States will not allow cartilage repair for patients with BMI greater than 30; for other carriers the cutoff is BMI of 35. Further research on the correlation between weight and progression of cartilage damage is necessary.

Patients who are taking medications for depression or anxiety and who have addictive baseline behavior patterns, such as alcohol consumption, smoking, or narcotic usage for pain outside of the postoperative setting, tend to demonstrate difficult postoperative patient management patterns. These factors must be delineated preoperatively and addressed individually. Providing preoperative counseling and maximizing medications for patients who have depression and anxiety in order to improve their postoperative sense of well-being and compliance is important. I do not operate on patients who are taking narcotics for baseline pain management of chondral defect or osteoarthritis until they are weaned off to a minimum baseline amount of narcotics that will allow good postoperative pain management. Smoking has demonstrated an adverse effect on bone healing and spinal fusions, long bone fractures, and trauma and on proteoglycan formation during cartilage healing. For this reason, we do not offer biologic repair to smokers until they have completed a smoking cessation program. If patients are unwilling or unable to stop smoking and they are at the transition age for a prosthetic reconstruction, then a unicompartmental, bicompartmental, or total knee arthroplasty is recommended.

Critical Cartilage Defect Size

Cartilage defects may be present and minimally symptomatic if the defect is small or the activity level is insufficient to cause progression of disease. Previous studies have reported that 2-cm² lesions coexist without degenerative changes in the knee up to 4 years after onset of symptoms.^7,8 More recent studies have shown no difference in clinical outcomes in anterior cruciate ligament–injured and stabilized knees with 2.1-cm² chondral defects at 15 years compared with controls in 36 knees.⁹ This finding supports the idea that progression of lesions smaller than 2 cm² is unlikely and that 2 cm² may represent a critical defect size. Based on these studies, early algorithms delineated 2 cm² as a small defect.^10–12

A critical size defect is considered a defect that shoulders the subchondral bone well from stimulus, thus lessening the symptoms from subchondral bone nerve stimulation and the abrasive effects of subchondral bone on the opposing articular cartilage and therefore the development of bipolar changes. A larger defect that is poorly shouldered will damage the opposing articular surface, resulting in progressive joint space cartilage loss, will remain symptomatic, and will enlarge quickly because of the excessive force on the edges of the defect. Figure 4–3 demonstrates this principle, which we described previously.¹²

Figure 4–3 A small well-shouldered chondral defect on the left prevents damage to the opposing surface because the shoulders of the defect support the subchondral bone. However, the defect on the right excessively overloads the shoulders, leading to premature breakdown of the supporting surface with abrasive changes developing on the opposing tibial surface. Persistent symptoms and degenerative changes are likely in this situation. A repair tissue that stabilizes the small defect usually is adequate. A repair tissue that simulates the normal viscoelastic mechanical properties of hyaline cartilage in the larger defect is necessary if the repair is to allow high-demand activities and be durable.

A relatively small defect that is symptomatic may be either treated by arthroscopic debridement of the unstable margins and then left alone, or stabilized with a repair tissue of fibrocartilaginous or hyaline cartilage. However, a larger poorly shouldered chondral defect will require a repair tissue with the same or nearly the same viscoelastic and mechanical properties as normal hyaline cartilage (Figure 4–4). Procedures that may produce hyaline-like cartilage for this situation are discussed in the remainder of this chapter (Figure 4–5).

Figure 4–4 A, Articular cartilage can be thought of as a viscoelastic mechanical tissue that integrates into the subchondral bone, allowing force transmission through an “osteochondral unit.” Restoration of the osteochondral unit via cartilage repair is the goal. B, Type II collagen, unique to articular cartilage, is arranged vertically. It then is anchored to the subchondral bone at the level of the tidemark of articular cartilage, running parallel to the articular surface and forming a regularly arranged scaffold that is well bonded to the bone and produces the framework for articular cartilage (arcades of Benninghoff). Characteristic deep middle and superficial layers of cartilage cells with their distinct behavioral properties are shown on the right. C, Schematic diagram of cartilage layers.

Figure 4–5 Proteoglycans produced by articular chondrocytes are highly negatively charged, attracting and binding to positively charged water molecules and forming a very resilient and unique viscoelastic mechanical tissue. In order for a tissue to withstand large mechanical compressive, torsional, and shearing forces, a reparative tissue that is hyaline-like is required. This is the goal of cartilage repair for large lesions.

Prevalence of Articular Cartilage Injury

In making recommendations to the patient, it is important to recognize the defects that are causing symptoms.

The spectrum of disease entities that cause damage to the articular cartilage ranges from single, focal chondral defects to more advanced degenerative disease. Focal chondral defects result from various etiologies. An approximately even number of patients have reported a traumatic versus an insidious onset of symptoms. Athletic activities are the most common inciting event associated with the diagnosis of chondral lesions.¹³ Traumatic events and developmental etiologies such as osteochondritis dissecans predominate in younger age groups. Several large studies have found high-grade chondral lesions (Outerbridge grades III and IV; Figure 4–6) in 5% to 11% of younger patients (<40 years) and in up to 60% of older patients.^13–15 The most common locations for these defects are the medial femoral condyle (up to 32%) and the patella.^14,15 Most are detected incidentally during meniscectomy or anterior cruciate ligament reconstruction.^13,16 Many of these defects are incidental in nature and asymptomatic.

Figure 4–6 Modified Outerbridge classification. Grade 1: intact articular cartilage with softening of the surface. Grade 2: fissuring of the surface up to 50% of the thickness of the articular cartilage. Grade 3: fissuring to the subchondral bone. Grade 4: exposed bone with undermining of cartilaginous tissue.

(From Ref. 40.)

The Asymptomatic Defect

The patient may have a known cartilage defect that is relatively asymptomatic. The question then becomes, “Will the lesion progress over time?” I have counseled patients in this situation to modify their activities to avoid impact and torsional sports and to cross-train with activities such as cycling, swimming, elliptical trainer, and upper-body weight training. These patients are followed-up with annual high-resolution MRI scans to determine whether the defect size is enlarging (Figure 4–7

Related posts:

Chondral Injury and Osteoarthritis: The Impact of Articular Cartilage Lesions Use of Fresh Osteochondral Allograft for Chondral and Osteochondral Defects in the Knee Patient-Specific Unicompartmental and Bicompartmental Resurfacing Arthroplasty Femoral Varus Osteotomy Tibial Osteotomy Patellofemoral Malalignment, Tibial Tubercle Osteotomy, and Trochleoplasty

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