Orthopedics - Oleksa A.P. 2006

Joint Diseases
Degenerative and Dystrophic Joint Diseases
Primary Chronic Gonarthrosis

Primary chronic degenerative-dystrophic lesions of the knee joint rank second in frequency of occurrence. Studies of knee joint specimens have shown that 60% of people over 70 suffer from gonarthrosis (Freeman M.A.R., 1980; Mohr W., 1993). It can be estimated that several million people in Ukraine require medical care due to pain and impaired lower limb function caused by gonarthrosis.

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Fig. 331. Protrusive coxarthrosis of the left hip joint.

Although in most patients the cause of primary gonarthrosis cannot be definitively established, the onset of the disease may be promoted by genetically inherited factors, such as abnormal articular Cartilage architecture, which under normal loading conditions can undergo degradation and cause osteoarthritis. Freymann points out that the harmful factor responsible for breaking down articular cartilage—initially as a localized lesion and later as widespread damage to all joint structures—remains unknown to this day.

It is believed (Ahlbäck S., 1968; Buckwalter J., Mankin H., 1997) that microtrauma or a single acute injury can disrupt The Structure of articular cartilage, whereas Skowроnski J. (1994) attributes this destruction to impaired cartilage Nutrition.

Mechanical overload of specific areas of the knee joint is known to play a role in The Development of gonarthrosis, potentially driving cartilage destruction. Golec E., Widawski A. (1997), and Popko J. (1990) suggest that normal recesses of the articular cartilage contain synovial fluid that becomes trapped during loading, thereby causing the fluid to loosen and fibrillate the cartilage tissue.

Buckwalter and Mankin (1997) argue that the primary pathomechanical factor involves repetitive overloads that cause microfractures of the subchondral bone trabeculae. Deprived of reliable structural support from Collagen fibers, the articular cartilage subsequently breaks down.

Many researchers (Freeman M., 1980; Gentry C. et al., 1995; Hauselmann H., Muff L., Stucki G., 1996, among others) believe that biochemical disturbances precede cartilage damage. Mechanical stress triggers biochemical alterations in the cartilage, exposing the Extracellular matrix, chondrocytes, and lymphocytes to synovial fluid. Wear debris from the articular cartilage induces an inflammatory response in the synovial membrane, followed by an immunological reaction characterized by the release of lytic Enzymes from synovial Cells, which further degrades the cartilage.

Some recent publications indicate that gonarthrosis may be triggered by extra-articular factors, particularly neuromuscular ones. As a person ages, the biomechanics of knee movement change, and Muscle weakness develops as a protective mechanism for the knee (Hunter W., 1994; Krause K., Neumann H., Roth N., Brosz M., 1995).

It is also suggested that gonarthrosis is associated with impaired Proprioception in the knee and altered Innervation of the anterior cruciate ligament, and that any disruption in neuromuscular control can contribute to the development of gonarthrosis.

The exact metabolic changes occurring in Proteoglycans, as well as the specific defects in their synthesis or breakdown, remain unclear. However, the majority of authors have demonstrated a reduced glycosaminoglycan content in degenerated cartilage affected by gonarthrosis (Heilmann H., Lindenhayn K., Walther H., 1996; Michalski P., 1997).

The initial site of articular cartilage injury may be either its matrix or its cells. An example of matrix damage is degenerative changes observed in patients with a congenital type II collagen defect, whereas rapidly progressive osteoarthritis following subchondral osteocyte osteonecrosis serves as an example of cellular injury (Diamond I., Linder J., Mosby, 1996; Buckwalter J., Mankin H., 1997; Hauselmann et al., 1996).

The early stage of the disease involves the fibrillation and destruction of articular cartilage, leading to exposure of the subchondral bone plate. Concurrently, immunological and metabolic processes responsible for biological repair take place. These two processes intertwine, making it difficult to determine when one dominates over the other.

According to Anderson's Pathology (Diamond I. et al., 1996), the histological and molecular alterations characterizing the progression of knee osteoarthritis can be divided into three phases.

In the initial (preliminary) phase, damage to the cartilage matrix by mechanical or biochemical factors induces cellular proliferation. This reaction triggers the release of lytic enzymes. Occasionally, subchondral bone injury may precede Changes in the articular cartilage, and the deposition of microcrystals within joint Tissues can act as a trigger initiating the pathomechanical degenerative-dystrophic process. Immunological processes within the degenerated articular cartilage also play a significant role.

In the second phase, degenerative-dystrophic changes in the articular cartilage and bone progress alongside repair and remodeling phenomena within the areas of cartilage defects. Proliferation of bone-forming tissue originating from the Bone Marrow can be observed in the damaged areas of the articular surface.

In the third phase, the accumulation of synovial cytokines and inflammatory mediators continues, playing a crucial role in The formation of sclerotic bone and marginal osteophytes characteristic of knee osteoarthritis (Kellgren J., 1965).

It should be noted that the composition of synovial fluid changes in osteoarthritis. Normally, the knee joint contains (6.7 ± 2.3) ml of synovial fluid. This fluid is a mixture of Blood Plasma filtrate passing through the capillaries of the synovial membrane and products secreted by synoviocytes (hyaluronic acid).

In asymptomatic knee osteoarthritis, the volume of synovial fluid doubles, and in classic cases, it increases several-fold (up to (24.2 ± 16.3) ml). The synovial fluid becomes turbid, rich in cells (up to 5–10 thousand per 1 mm³), exhibits an acidic pH (7.1–6.8), shows a decreased glucose level, and an increased protein concentration (Golec E., Widawski A., 1997).

Gonarthrosis causes alterations in periarticular tissues (bursae, ligaments, and adjacent tendons), leading to joint deformity and restricted range of motion. In turn, compensatory and subsequently fixed flexion contractures impair limb function, negatively affecting the ligamentous apparatus and knee bursae (Kwiatkowski K., Siwek W., 1995). The anterior cruciate ligament of the knee is particularly prone to destruction, which may manifest as joint instability.

Clinical manifestations of idiopathic gonarthrosis depend on the stage of the degenerative-dystrophic process, as the condition progresses slowly. In case history taking, it is essential to clarify The Nature of the pain, joint stability, range of motion, and the patient's functional capacity for weight-bearing daily activities. Typically, pain at the onset of the disease occurs after joint overload and subsides with rest; later, the pain becomes constant, although its localization and character may vary.

Knee pain in individuals over 60 is a hallmark of a degenerative-dystrophic process. The pain is caused by changes in intra-articular pressure and irritation of nerve endings in the synovial membrane and Joint Capsule, as well as irritation of nerve fibers in the subchondral bone in areas of cartilage defects.

A characteristic feature is "start-up" pain upon taking the first steps after sleeping or prolonged sitting. Pain may intensify upon pressure over the joint space line. Occasionally, signs of synovitis, mild local hyperthermia, and an inability to fully extend the lower leg due to an antalgic contracture can be detected. Over time, quadriceps atrophy, limb muscle weakness, and knee deformity develop.

Degenerative-dystrophic changes in the joint are focal in nature, creating discrepancies between the clinical and radiological signs of the disease. In the early phase of gonarthrosis, all Clinical symptoms of the disease are present, while radiographs reveal no obvious joint pathology.

Later, cartilage defects manifest radiographically (Fig. 332) as joint space narrowing. The deterioration of the Shock-absorbing Properties of the cartilage leads to sclerotic changes in the subchondral bone plate. Subsequently, marginal osteophytes and bony growths develop at ligament and tendon insertion sites, accompanied by cystic changes in the cancellous Bone Structure, particularly within the Tibia.

Fig. 332. Radiographs in two projections of osteoarthritis (degenerative joint disease) of the knee joint.

The progression of these pathological changes can be radiologically classified into four stages according to Kwiatkowski (1998), who modified the Kellgren grading system.

Stage I — without narrowing of the tibiofemoral and patellofemoral spaces, accompanied by minor marginal osteophytes. These signs may be equivocal during Diagnosis.

Stage II — noticeable narrowing of the tibiofemoral and patellofemoral joint spaces and more pronounced marginal bone overgrowths. A marginal ossicle is visible on the upper border of the Patella at the insertion site of the rectus femoris muscle.

Stage III — clear marginal osteophytes are visible in the regions specified in stage II, along with subchondral bone sclerosis. In the lateral projection, the osteophyte of the superior pole of the patella and the narrowing of the space between it and the Femur are clearly distinguishable.

Stage IV — significant narrowing of the joint space, deformation of the articular surfaces with prominent marginal bone outgrowths, marked sclerosis, and cysts in the subchondral bone. Tibial subluxations may occur, as well as deformation of the patellar articular surface, sometimes accompanied by loose osteochondral bodies within the joint (Fig. 333).

In the USA, Dihlmann's radiological Classification of gonarthrosis is commonly used:

Grade I — chondromalacia and initial Bone tissue response; symmetrically narrowed joint space, while in valgus or varus knee deformity, osteophytes appear unilaterally along the margins of the articular cartilages of the intercondylar eminence of the tibia and the patella;

Grade II — intensification of the previous features with destruction of the subchondral bone tissue leading to cystic changes;

Grade III — progressive joint destruction with deformation of the articular bone ends and subluxation. Pronounced osteophytes along the margins of the articular cartilage, chondromatosis, and signs of ossification in the periarticular soft tissues.

To obtain technically sound radiographs that accurately reflect the state of the knee joint in gonarthrosis, Ahlback S. (1968), Gibson P., Goodfellow (1986), and Swiatkowski J. (1998) suggest adhering to three conditions: 1) the central X-ray beam must pass perpendicular to the subchondral bone layer; 2) the joint must be positioned (extended or flexed) such that the central beam passes perpendicular to the areas of greatest articular cartilage destruction; 3) at least one radiograph must be taken in a weight-bearing standing position on the affected limb.

Greenspan A. (1988) points out that standard radiographs in only two projections of a single knee joint generally fail to reveal pathological changes in the Cytology/cytology/16.html">Early stages of the disease. To properly assess the nature of joint involvement, it is advisable to perform knee radiography in three or even four projections, and invariably conduct comparative radiographs of the contralateral knee (Ahlback S., 1968; Gyrecki A., Ku W., Swiatkowski J., 1990).

More informative data can be obtained via Magnetic Resonance imaging (MRI) of the knee, which can detect early pathological changes not only in the subchondral bone layer but also in the articular cartilage and adjacent soft tissues. However, this diagnostic modality is not yet widely used due to equipment scarcity and high examination costs.

Fig. 333. Radiograph of osteoarthritis of the knee joint with loose intra-articular bodies prone to entrapment.

Diagnostic knee arthroscopy is now widely utilized and remains the most informative method, as it allows for the visual inspection of all intra-articular structures.

Treatment. The optimal choice of treatment method depends on the stage and progression of gonarthrosis, its clinical manifestations, and the patient's age. In the early stages, conservative treatment Methods are employed; although they cannot halt the degenerative-dystrophic process, they can slow its progression and prevent premature disability.

Conservative management should be comprehensive, incorporating limb unloading, therapeutic exercise (kinesiotherapy), muscle massage, physical and balneotherapy, pharmacological agents, and sanatorium-resort treatment.

To unload the limb, patients should use a cane, apply cuff traction to the lower leg before bedtime, and use crutches in cases of persistent pain. To maintain muscle strength and prevent atrophy, patients are prescribed active Therapeutic Exercises without limb loading or during simultaneous traction, along with muscle massage, particularly targeting the quadriceps. These exercises must be performed regularly before getting out of bed and after prolonged sitting. Gymnastic exercises are advantageously supplemented with hydrogen sulfide or radon baths in rehabilitation clinics or resort settings. Swimming in a pool is also beneficial.

The therapeutic regimen includes physical therapy and balneotherapy modalities. The simplest approaches for home use include Solux lamps, paraffin-ozokerite Applications, and thermal compresses.

Physiotherapy departments and rehabilitation centers utilize diadynamic currents, Electrophoresis with a 1% novocaine solution, ichthammol, ronidase, etc., pain-relief galvanization, baths, and mud therapy. If pain persists, ultrasound therapy—particularly combined with magnetotherapy—is beneficial.

The efficacy of laser therapy has been validated by our department, which pioneered its medical application in 1969 for treating patients with osteochondrosis and osteoarthritis. Clinical and Laboratory studies (by Moroz O.) have demonstrated that, by acting on reflexogenic zones, local helium-neon laser irradiation improves microcirculation and metabolic processes, enhances collagen and Protein Synthesis, and accelerates cellular proliferation.

Pharmacotherapy for osteoarthritis aims to reduce pain and clinical symptoms while slowing the progression of the degenerative-dystrophic process in the affected joint.

Standard practice involves The Use of non-opioid analgesics (such as Tylenol or Panadol) and anti-inflammatory drugs, which are widely available and heavily promoted by global pharmaceutical companies.

Currently, non-steroidal anti-inflammatory drugs are widely used, administered in courses. They can be divided into several groups:

1) butylpyrazolidine derivatives (butapyrazole, percluzone);

2) acetic acid derivatives (diclofenac, indomethacin, methindol, naclofen, voltaren, revodin);

3) oxicams (piroxicam, feldene);

4) propionic acid derivatives (apranax, ibuprofen, naprosyn, profenid, surgam);

5) other agents (benalgin, relifex, etc.).

Clinical observations indicate that the drug and its dosage should be selected individually, taking into account the highest efficacy during treatment courses with various medications. However, a dramatic, visible therapeutic effect in osteoarthritis is not always achieved with these drugs.

Clinical practice shows that when using a new medication, over 60% of patients experience improvement if they are convinced of its high efficacy (Traut E.F., Passarel E.W., 1957; Gentry C., Blower P., Spangler R., 1995).

Steroid Hormones, which inhibit prostaglandin synthesis and provide anti-inflammatory effects, are effective; however, they should not be used in osteoarthritis. Their intra-articular administration carries a risk of Purulent Arthritis due to potential aseptic breaches, and repeated injections can accelerate cartilage degradation or even lead to aseptic osteonecrosis.

Nowadays, intra-articular injections of hylan (or hyalgan) are widely used; it acts as a synovial fluid substitute, reducing friction between articular surfaces and providing long-lasting pain relief. Nevertheless, it is ineffective in cases of severe articular cartilage destruction caused by osteoarthritis.

Surgical treatment of idiopathic gonarthrosis.

Progressive knee pain and impaired limb function force patients to seek continuous conservative treatment, which eventually becomes ineffective and unhelpful. To address this, Magnuson (Magnuson B.P., 1941) proposed an open arthrotomy with knee joint debridement, a Procedure that later lost popularity.

If neither the patient nor the physician is yet ready to resort to radical surgery, a minimally invasive arthroscopic procedure can be performed as both a diagnostic and therapeutic tool (lavage, debridement, drilling).

Knee arthroscopy was first described by Burman M.S., Finkelstein H., Mayer L. (1934).

Arthroscopy is performed under anesthesia. To prevent intra-articular bleeding, a pneumatic tourniquet is sometimes used during surgery, though continuous joint irrigation is preferred. About 5-6 liters of saline solution are prepared beforehand to ensure clear visibility of all joint compartments during continuous irrigation.

To introduce the arthroscope (with a 30° lens) and necessary manipulative arthroscopic instruments (hook, shaver, motorized burr, grasping forceps, etc.) into the joint, three 1-centimeter Skin incisions are made, and surrounding tissues are punctured with a trocar on both sides of the patellar ligament or directly through it. A third, auxiliary suprapatellar incision is made for continuous joint irrigation (Fig. 334).

Knee arthroscopy allows for a detailed examination of intra-articular structures and helps determine the appropriate scope of intervention. Depending on the severity of gonarthrosis, various arthroscopic surgical Procedures can be performed.

Technically, the simplest procedure is joint lavage (washing out the knee joint cavity), which removes synovial fluid containing lysosomal enzymes and small free fragments of destroyed articular cartilage.

Currently, intensive knee irrigation is given greater significance, as patients experience substantial long-term relief (Dandy D.J., Liveseley P.J. et al., 1991; Gibson J.N.A. et al., 1992).

Special forceps can be used to remove larger osteocartilaginous loose bodies, or to fragment and wash them out. A shaver is used to excise damaged meniscus areas and perform partial synovectomy of hyperplastic regions. If an articular cartilage defect is identified, it is debrided, the joint surface is smoothed, and the Base of the defect is drilled in multiple places with a Kirschner wire down to the bleeding cancellous bone. This enhances local repair processes and stimulates the formation of fibrocartilage, which, unfortunately, lacks the necessary biochemical and biomechanical properties. Intra-articular osteocartilaginous growths can also be arthroscopically removed, although this yields limited overall benefit.

The surgery concludes with wound closure (placing single sutures), application of an aseptic dressing, and a limb-immobilizing brace or "CPM" splint. Postoperatively, cold therapy (ice, crio/cuff "An-cast", etc.) is applied to the knee for two days, and mild anticoagulants are prescribed if necessary.

It should be noted that such arthroscopic surgery yields good results in 50–80% of operated patients for a duration of 2–5 years (Bert J.M., Maschka K., 1989; 1990; Baumgaer M.R., Connon W.D., 1990; Burks R.T., 1990; Downs S., 1997, et al.), although it does not restore the smooth hyaline surface of the articular cartilage.

Fig. 334. Insertion of the arthroscope and arthroscopic instruments into the knee joint.

The best debridement results are achieved in young individuals with mild degenerative changes in the knee, without joint instability or limb axis malalignment (Ruszkowski K. et al., 1998).

Currently, the feasibility of expanding The Scope of arthroscopic surgical interventions for gonarthrosis is being considered, such as closing articular cartilage defects with grafts, employing lab-expanded chondrocytes, and prospective methods yet unknown to us.

Contraindications to arthroscopic surgery include severe degenerative-destructive changes in the articular cartilage with marginal osteophytes, arthrogenic contracture, active inflammation in the knee or foci of infection elsewhere in the body, as well as cases where the anesthesiologist identifies various contraindications to anesthesia.

In cases of persistent pain and impaired lower limb function resulting from gonarthrosis, radical surgeries are now employed. For manual laborers who are forced to constantly overload their knee joints, arthrodesis should be the procedure of choice in unilateral gonarthrosis. With an ankylosed knee, the patient can fully bear weight on the operated leg, which reduces the load on the contralateral limb and prevents the development of arthrosis.

Surgical technique. The operation is performed under general anesthesia with a thigh tourniquet. The knee joint cavity is opened via a Payr incision by dissecting the patellar ligament proper and removing the fat pads. The soft-tissue flap with the patella is retracted proximally, the joint capsule and ligaments are excised, and the articular ends of the bones are mobilized. Next, protectors for the popliteal neurovascular bundle are inserted, and the articular ends, including the patella, are conservatively resected down to the cancellous bone structure.

Resection is performed so that the tightly apposed ends maintain the tibia along the correct axis, slightly flexed (5–10°). The apposed bone ends are fixed in a stable position using the Ilizarov apparatus or rod fixators without a plaster cast, or by other methods (rods, pins) supplemented with a long leg plaster cast (Fig. 335).

The surgical wound is closed and drained for 24–48 hours. The advantage of hardware fixation methods is that patients can bear measured weight on the leg after three weeks, while full weight-bearing is permitted one and a half months post-surgery. The apparatus is removed after radiological confirmation of bony ankylosis.

In cases of bilateral gonarthrosis in manual laborers, one knee joint undergoes arthrodesis while the other is arthroplastied. Bilateral knee arthroplasty is performed in patients over 60 years of age who will not overload their legs. Given that the articular surfaces of both bones are typically affected in gonarthrosis, bicompartmental (total) knee arthroplasty is generally required.

Arthroplasty technique. The operation is performed under anesthesia with a thigh tourniquet. The joint cavity is opened via a vertical parapatellar incision, and its condition is assessed. If a preserved, healthy articular cartilage is found on the femur, one can be limited to tibial arthroplasty alone, though this occurs rarely.

Fig. 335. Various methods of knee joint fixation during arthrodesis surgery.

With the knee flexed, the articular ends of the tibia and femur are mobilized from soft tissues while simultaneously excising the synovial membrane, menisci, and any remaining cruciate ligaments. A rod is driven from the intercondylar region of the femur into the medullary canal, upon which a standard template is placed. Using the template, the articular end is resected in three planes (Fig. 336) that precisely match the planes of the inner surface of the femoral prosthesis component (Fig. 337).

Next, a canal is formed in the bone matching the shape of the prosthesis stem, its correct placement is verified, adjusted if necessary, and bone cement is mixed ex tempore. The canal is filled with the cement, and the prosthesis stem is driven in so that the endoprosthesis closely apposes the bone throughout its entire length.

Fig. 336. Resected femur in three planes relative to the planes of the femoral prosthesis component.

Subsequently, using a second template while maintaining normal limb axis alignment via a guiding device, the articular end of the tibia is resected (Fig. 338), and the tibial component of the endoprosthesis is cemented into the prepared canal. The direction of movement and function of the endoprosthesis are verified, and the wound is closed in layers and actively drained with a thin polyethylene tube for 24–48 hours. The limb is immobilized in a standard knee immobilizer until the wound heals. Wound dressing and pad replacement are mandatory on the day following surgery.

Figure 311 shows a radiograph of an arthroplastied knee.

After suture removal, the patient begins mobilizing the operated knee. The patient is allowed to bear weight on the limb and use a cane while walking after 2.5–3 months.

Surgery for gonarthrosis on the second knee can be performed 6 months later, that is, after complete functional recovery of the operated leg.

In relatively young, physically active individuals, arthroplasty has limited indications; therefore, operations based on autologous chondrocyte or mesenchymal Cell transplantation for minor cartilage destructions and defects have begun to be developed.

Peterson's animal experiments (1984) prompted Brittberg et al. (1994) to introduce this method into clinical practice, applying it in 23 patients with focal cartilage defects following trauma and resulting from König's disease.

During this procedure, 300–500 mg of cartilage is arthroscopically harvested from a non-weight-bearing area of the medial femoral condyle. Chondrocytes are then isolated from the matrix using collagenase and deoxyribonuclease and expanded in vitro for 2–4 weeks. The obtained material is transplanted into the cartilage defect, cleaned down to the bone, following open arthrotomy. For this purpose, a free periosteal flap is harvested from the tibia, used to cover the defect by suturing it to the cartilage margins, after which chondrocytes are injected underneath.

Fig. 337. Components of prostheses for knee arthroplasty.

Fig. 338. Direction of tibial resection (a) relative to the planes of the tibial and femoral endoprosthesis components (b).

In 1998, Peterson presented the outcomes of autologous chondrocyte implantation in 213 patients. The majority of cases showed good to excellent results, leading him to consider this approach highly promising.

Simultaneously, other techniques for articular cartilage defect repair were under development. Clinical practice saw the Introduction of carbon fiber scaffolds, periosteal or osteochondral autografts, as well as osteochondral allografts.

Treatment of cartilage defects using carbon fiber scaffolds. This therapeutic method is based on creating a matrix—essentially a scaffold—for Connective Tissue cells that progressively fill the pores between the fibers of the implanted carbon material. The fibers stimulate the synthesis of collagen fibers, which subsequently grow into the network.

Minns R. (1989) and Pongor P. (1992) described the results of this method in over one hundred patients. Brittberg M. (1994) reported the use of porous carbon scaffolds in 37 patients suffering from knee osteoarthritis. The treated patients ranged in age from 25 to 53 years.

These authors noted that the application of carbon implants for articular cartilage defects resulted in pain relief and significant functional improvement of the knee joint in 70–83% of the treated patients during the follow-up period ranging from 33 to 63 months post-surgery.

The positive effects of porous carbon fiber transplantation for repairing articular cartilage defects were also reported by Ku W. M. and Strzelczyk P. (1998).

Periosteal transplantation for cartilage defects. The use of periosteal grafts to repair articular cartilage defects was described by Homminga G. N. (1990). He treated defects measuring 2–3 cm² using periosteum harvested from the Ribs. During patient follow-up, radiographic evidence of graft ossification was detected two years post-surgery. This endochondral ossification progressed and became the cause of unfavorable outcomes five years after surgery (in 7 out of 10 treated patients), whereas results were favorable During the first three years (Ku W. M., Strzelczyk P., 1998). O'Driscoll S. W. (1988) likewise reported unsatisfactory outcomes in 40% of patients following this procedure.

Consequently, cartilage defect repair using periosteum has been deemed inappropriate due to progressive endochondral ossification.

Repair of cartilage defects using osteochondral autografts. This method is primarily indicated for relatively small cartilage defects typically associated with osteochondritis dissecans and is less suitable for osteoarthritis.

The first reports on using osteochondral autografts for articular cartilage defects measuring 10 to 22 mm were published by Dobie V. (1996). He harvested 3–5 osteochondral autografts from a non-weight-bearing area of the femoral condyle articular cartilage and implanted them into the defect. At 6 months post-surgery, magnetic resonance imaging (MRI) confirmed graft integration with the bone.

Hangody L. (1997) applied this surgical technique in 169 patients, utilizing 1 to 18 autografts per procedure. In 44 patients with small defects, the surgery was performed arthroscopically. Depending on the defect Location, weight-bearing was permitted 4–6 weeks post-surgery. Both the physician and the patients were satisfied with the clinical outcomes.

During second-look arthroscopy, Hangody observed incorporation of the autografts with fibrocartilage filling the gaps between them, while the articular surface in the grafted area was histologically classified as hyaline cartilage.

Similarly, Trzaska T. (1992) achieved good to excellent results in 79% of patients treated with this method, with a 100% success rate among patients aged 19–25 years.