Ligaments are connective tissues mainly consisting of collagen fibres [1, 77]. They are bone-to-bone connections that contribute to load transfer, guiding joint motion and provide joint stability [1, 77]. The primary ligaments of the knee joint are the cruciate and collateral ligaments. The anterior cruciate ligament (ACL) connects the inner surface of the lateral femoral condyle to the medial part of the anterior intercondylar eminence of tibia. The posterior cruciate ligament (PCL) connects the posterior part of the intercondylar notch of the medial femur to the posterior intercondylar eminence of the tibia. The medial collateral ligament (MCL) connects the medial femoral epicondyle to the medial tibia∼5 cm below the joint line. The lateral collateral ligament (LCL) connect the lateral femoral epicondyle to the head of the fibula.
The ACL primarily restricts anterior translations and internal rotations of the tibia with respect to the femur, while the PCL restricts posterior translations and external rotations [1, 85]. The dynamic stability of the knee joint is provided by the interaction between ACL and PCL. MCL and LCL primarily restrict valgus and varus rotations respectively [42, 51, 86].
3 Knee osteoarthritis
Knee OA is characterized by a progressive loss of articular cartilage from joint surfaces, subchondral bone cysts and osteophyte formation. OA affects all synovial joint tissues: cartilage, menisci, ligaments, synovium, muscles, bones and causes joint pain during motion. Typically, OA is seen in the foot, knee, hip, spine or hand joints, but can affect all synovial joints.
Some of the first signs of OA are collagen network fibrillation, elevated water content, and a reduction of PG content starting initially from the superficial zone.
These compositional and structural changes lead to increased permeability and decreased cartilage stiffness. As the disease progresses, the cartilage surface starts to degrade, which leads to the presence of cartilage fragments in the joint space. At the end stage of OA, the articular cartilage surface has become fully degraded, causing bone-on-bone contact. This leads to severe pain and joint stiffness.
3.1 RISK FACTORS FOR OA
There are several risk factors that increase the likelihood of knee OA. A brief overview of some of the risk factors and their relationship to knee OA is presented below.
Aging. There is increased incidence of OA in subjects over 50 years. With age, there are morphological and biomechanical changes in articular cartilage, such as decreased collagen concentration, shorter protein cores and increased water and PG content [1, 77, 87]. In addition to alterations in articular cartilage, with age there are changes in muscle (sarcopenia), bone (osteopenia, osteoporosis), fat (increased fat deposits) and the nervous system (altered proprioception). These all play a role in the development of knee joint OA [88].
Gender. There are studies reporting markedly higher incidence of OA in female subjects, especially when associated with age [89, 90], weight [91] and knee injuries [12, 92]. Moreover, there are gender-based gait differences in osteoarthritic knee joints [93, 94].
Knee alignment. In theory, a shift from a neutral alignment of the knee affects the load distribution. Some studies identified knee malalignment as a potential predictor of OA [95–99]. However it is still unknown whether malalignment precedes the development of OA or it is a direct result of cartilage loss [100, 101].
To achieve a neutral alignment in patients with knee malalignment, tibial osteotomy is typically performed [102, 103]. In tibial osteotomy, a wedge of tibial bone is surgically removed. However, several factors such as gender, surgeon experience, pain medication intake and postoperative complications greatly affect the individual’s susceptibility to OA onset and development [104–106].
Disuse. As a result of chronic bed rest or sedentary life, there is a drastic change in articular cartilage, bones and muscles. In articular cartilage, there is a reduction in the amount, size and synthesis of PGs, as well as an increase in cartilage surface fibrillation [77]. In weight-bearing bones, there are substantial changes in bone geometry and composition [77]. As a result of disuse, the muscles
undergo a rapid and significant atrophy with no change in muscle fibre numbers [77]. When combined together, these changes can lead to abnormal joint biomechanics and stresses and strains experienced by articular cartilage [15–17, 107].
Weight. A high body mass index (BMI) and obesity significantly increase the risk of developing OA [108–110]. Excessive impact and cumulative loads, decreased muscle strength and altered biomechanics may promote structural joint damage [111]. Moreover, obesity can trigger metabolic responses that inhibit matrix synthesis and induce cartilage degeneration [112]. The primary and most effective intervention for obese OA patients is weight loss. It was shown that a reduction of 2 units of BMI could decrease the probability of developing knee OA by 50%.
Weight loss has been shown to reduce both the extent of inflammation and the magnitude of knee joint loads [113].
3.1.1 Traumatic joint injuries and surgery
Traumatic knee joint injuries include meniscal tears and cruciate and collateral ligament ruptures. These injuries are typically seen in sports activities that involve jumping, pivoting or cutting, such as football, basketball or downhill skiing.
Treatment. Since the ACL plays and important role in knee joint stability, ACL injuries are commonly treated conservatively or surgically. In the conservative treatment, several weeks of rehabilitative therapy (exercises) are performed under the supervision of a physical therapist. The goal of rehabilitative therapy is to reduce pain, swelling, strengthen muscles and restore the knee joint’s full range of motion. In the surgical treatment, the damaged ACL is replaced with a tendon graft, which can be harvested from another part of the patient knee (autograft) or from a deceased donor (allograft). Typical tendon grafts used in ACLR are from the patellar, quadriceps or Achilles tendons. To accurately position the tendon graft, tunnels are drilled into the femur and tibia. The graft is then secured to the bone using fixation devices, such as screws. ACLR surgery is usually followed by progressive physical therapy to strengthen the muscles and improve flexibility [12, 114–116]. The aim of surgical treatment is to restore the knee joint stability and full range of motion, as the ACL resists anterior translations and internal rotations of the tibia.
There are two main treatment options for meniscal tears, depending on their severity, size and location: conservative and surgical. Conservative treatment is prescribed when the damaged tissue is small and is located on the outside edge of the meniscus. Conservative treatment techniques often include resting, ice (cold packs several times a day), using compression bandages and keeping the leg elevated to reduce additional swelling. The surgical treatment of meniscal injuries is typically done using arthroscopic surgery. Miniature surgical instruments and a miniature camera are inserted through small incisions in the knee. Then the damaged tissues are either trimmed away (partial meniscectomy) or repaired using sutures (meniscus repair).
Relationship with OA. There is an increased risk for the onset and development of knee OA as a result of meniscal tears [117–121] or ACL ruptures [122–124]. Furthermore, ACL injuries are often accompanied by meniscal tears, subchondral bone or cartilage damage, which further increase the susceptibility of OA [6, 7, 9, 114, 125–128]. It is unclear if conservative treatment of ACL ruptures is more suitable than surgical treatment, with several studies
showing little difference in OA susceptibility between the two [12, 115, 116].
Postoperatively, the incidence of knee OA was notably higher in patients with ACLR in both long-term [9, 11, 128–130] and short-term follow-ups [8, 14, 126] than in healthy controls. For meniscal tears, both conservative and surgical treatment options lead to increased OA susceptibility [119]. Postoperatively, the incidence of knee OA was higher in partial meniscectomy patients both in short and long-term follow-ups than in healthy controls [80, 131–136].
The increased susceptibility for OA development in patients with traumatic joint injuries may be due to altered biomechanics. The surgical interventions may not instantaneously stabilize the joint back to normal and may also cause short-term inflammation. For instance several studies report significantly different gait characteristics [92, 94, 137–139] in patients with ACLR than in healthy controls.
For ACLR patients, there are significant differences in both knee joint contact forces [140, 141] and muscle forces [16, 94, 142, 143] even at 1-year post ACLR surgery. This altered joint motion may lead to abnormal stresses and strains experienced by articular cartilage [15–17], which may increase the risk for the onset and development of knee OA.
3.2 RADIOLOGICAL EVALUATION METHODS OF OSTEOARTHRITIS