**1. Introduction**

Musculoskeletal injuries that disrupt the structure and function of diarthrodial joints can cause permanent biomechanical alterations and lead to a more severe, chronic condition. Despite advancements that have been made of restore tissue function and delay the need for joint replacement, there are currently no diseasemodifying therapies for osteoarthritis (OA). To reduce the risk of OA, innovative preventive medicine approaches have been developed over the last decade to treat the underlying pathology.

The lesions of the articular cartilage are a common disorder that with the aging of the population its prevalence is increasing. More than 500,000 procedures are performed for the treatment of articular cartilage-related injuries, and many of these procedures are repeated in the same patients. This demonstrates the ineffectiveness of this isolated procedure [1].

Hunter [2] noted that the cartilage, "once destroyed, is not repaired." Fact that keeps current. Some studies have shown an incidence of cartilage lesions greater than 65% in routine arthroscopy [3–6]. No procedure nowadays is reliable for the regeneration of articular cartilage. This is due to the complexity of its structure and functional properties, such as minimizing friction and increasing the contact surface area to decrease wear under load.

Cartilage lesions (9 mm or greater) have been reported to be biomechanically unstable with a high propensity of progression to degenerative osteoarthritis [7, 8]. The main characteristics of the clinical presentation are pain, loss of movement, and alteration of function. Various surgical procedure options can be used for treatment; this will depend on the location, size, and stage [9, 10].

Articular cartilage is composed of chondrocytes (5–10%), water (65–80%), collagen, smaller glycoproteins such as fibronectin and oligomeric cartilage proteins, and large negatively charged hydrophilic proteoglycans (aggrecan, hyaluronan). Four distinct zones are described microscopically.

 The superficial zone protects the deeper layers of shear stresses and composes approximately 10–20% of the thickness of the articular cartilage. The main collagen fibers found are type II and IX with a high number of flat chondrocytes. It is the layer that protects and maintains the integrity of the deeper layers, is in direct contact with the synovial fluid, and is responsible for most of the traction properties of the cartilage, which allows it to resist the pure, elastic, and compressive forces imposed by the joint.

The intermediate (transitional) zone provides an anatomic and functional bridge between the superficial and deep zones, accounts for 40–60% of the total cartilage volume, and contains thicker collagen proteoglycans and fibrils. Collagen is organized obliquely, and the chondrocytes are spherical and low density. The compressive forces mainly exhibit resistance.

 The deep zone is responsible for providing greater resistance to the compressive forces, since the collagen fibrils are arranged perpendicular to the articular surface. The deep zone contains collagen fibrils of larger diameter in radial arrangement, higher content of proteoglycans, and lower concentration of water. Chondrocytes are typically arranged in columnar orientation, parallel to collagen fibers, and perpendicular to the joint line. It represents approximately 30% of the articular cartilage volume.

The calcified layer plays an integral role in the attachment of the cartilage to the bone, anchoring the collagen fibers from the deep zone to the subchondral bone. There are few cells and the chondrocytes are hypertrophic [9, 11–13].

 Several factors are part of the etiology of the chondral or osteochondral lesion; among them are metabolic, such as obesity, alcohol abuse, and diabetes, as well as mechanical factors such as trauma, joint misalignment, and instability [12, 13].

Osteochondral lesions heal by formation of fibrocartilage secondary to the initial inflammatory response. Although mesenchymal cells produce collagen type I and II, the repair is mostly fibrocartilaginous in nature. The orderly structural organization of normal hyaline cartilage is lacking and results in early degradation and fragmentation. However, pure chondral lesions are painless and poorly repaired due to lack of vascularity [9, 14].

 Surgical and nonoperative procedures are employed in the treatment of cartilage lesions. The main objective goal is to reduce pain and restore function. Nonsurgical treatments include physical therapy, activity modification, braces and orthoses, weight loss, steroid injections, chondroitin sulfate, and viscosupplementation with hyaluronic preparations [15–20]. The operative treatment aims to improve joint function and congruence as well as prevent osteoarthritic damage in intact areas of cartilage. It may be divided into three techniques commonly performed to preserve the joint including bone marrow stimulation, cartilage repair, and cartilage regeneration.
