Varus or valgus malalignment of the lower extremity results in an abnormal load distribution across the medial and lateral tibiofemoral compartment. For example, a 4–6 % increase in varus alignment increases loading in the medial compartment by up to 20 % [3].

Articular cartilage and subchondral bone are subjected to an increased stress, suggesting that axial malalignment plays an important role in the development of early OA.

However, studies examining the relationship between malalignment and early knee osteoarthritis have produced conflicting results.

A possible relationship between the incidence of early osteoarthritic changes and axial malalignment is only supported by limited evidence so far.

In contrast, the correlation between the progression of early osteoarthritic changes and axial malalignment has been well established. Both conventional radiological and MRI [4] studies found that axial malalignment is a potent risk factor for progression of early osteoarthritic changes in patients with axial malalignment. Articular cartilage loss and subchondral bone changes may lead to an increased malalignment. Cicuttini et al. [5] reported that the degree of varus knee angle was associated with a reduction in the volume of both femoral and tibial articular cartilage in the medial tibiofemoral compartment of the knee over a 1.9-year follow-up period. Similar results were seen in the lateral tibiofemoral compartment.

The rationale for high tibial osteotomy (HTO) is slowing or preventing early osteoarthritic changes by restoring a more favorable biomechanical situation, thereby reducing local compartmental overload, via correction of malalignment. However, the long-term effectiveness of HTO for treatment of medial compartment osteoarthritis has not been experimentally confirmed to date.

Everything suggests that malalignment is related to increased occurrence and faster progression of osteoarthritic changes, and high tibial osteotomy shows promising results even though there is no evidence of such change prevention. Such practice must be studied deeper to increase our knowledge and to justify this practice.

Any substantial loss of meniscal tissue from injury or iatrogenic meniscectomy permanently alters knee joint biomechanics and biology [6]. Subtotal or total meniscectomy increases the risk of secondary osteoarthritic changes by a factor 14 when compared to matched controls [7], eventually resulting in radiographic changes in 30–70 % of patients [8]. The role of concomitant cartilage damage related to the trauma that resulted in meniscal injury in the first place, or of iatrogenic damage related to the meniscectomy procedures, has not been determined, but is likely to play a role as well. The younger the patients, the worse the outcomes, especially in those with associated articular comorbidities such as chondral damage, ligamentous instability, and malalignment [9].

Initially described as vestigial, nonfunctional tissue, the menisci have since been found to play a vital role in load transmission in the knee. They transmit 50 and 70 % of the medial and lateral compartment load, respectively, with the knee in extension. This increases to almost 85 % when the knee is flexed to 90° [10]. The menisci also serve as an important secondary restraint to anteroposterior joint translation in unstable knees, that is, knees with deficient anterior cruciate ligament. Biomechanical studies have demonstrated significant alteration in load transmission with meniscal deficiency or mismatch [9].

Biomechanical and animal models of meniscal repair demonstrated near-normal load transmission [11], providing a rationale for meniscal repair when possible. The same study, however, pointed out the challenges posed by radial tears, which even after successful healing demonstrated decreased contact area.

Clinical data reflect the biomechanical changes observed experimentally. Radiographic changes in the knee joint after meniscectomy were noticed as early as 1939; however, Fairbank was the first to describe in 1948 a consistent pattern of ridge formation, femoral flattening, and joint space narrowing in 107 patients that had undergone open, most likely complete meniscectomy [12]. Jackson in 1968 reviewed 577 meniscectomized knees, demonstrating increasing numbers of patients with degenerative changes and osteoarthritic symptoms with longer follow-up, reaching 67 and 33 %, respectively, at 30-year follow-up [13]. These findings were confirmed subsequently by multiple authors, supporting Fairbank’s theory that meniscectomy predisposes the knee to osteoarthritis, especially when concomitant injuries or abnormalities are present, such as instability or malalignment. Relatively few experimental studies on this subject have been performed in vivo besides Voloshin and Wosk [14] who were able to demonstrate a 20 % reduction in the shock absorption capacity of the knee after meniscectomy.

The changes in biomechanical and biological environment of the knee joint following loss of meniscal tissue, either traumatic or following meniscectomy, and the deleterious consequences of those changes on the articular cartilage are well known.

This leads to the meniscal transplantation rationale: to restore the optimal biomechanical environment that has demonstrated an improved contact area and peak stresses and a reduction in tibial translation and thus in ACL strains, being the menisci a secondary stabilizer of the knee.

Of course sizing, positioning, and fixation technique for meniscal transplants appear to have important impact on biomechanical results.

In literature, it is reported that even though degenerative changes were not avoided, they were reduced in comparison to meniscectomized controls.

Overall, patients needing a meniscal transplant without malalignment or following high tibial osteotomy had far better results.

Cartilage lesions should be evaluated carefully in order to assess their depth: they are divided into partial-thickness and full-thickness defects, plus osteochondral lesions.

Partial-thickness lesions are usually less symptomatic (symptoms are usually related to bone and periarticular tissue changes), and there is little evidence regarding their progression onto osteoarthritis, while full-thickness chondral or osteochondral lesions are believed to predispose to premature osteoarthritis [15–17].

This kind of lesions are of a common finding in asymptomatic patients (up to 20 % during arthroscopy and up to 40 % as MRI findings), and it is not clear which lesion and under which circumstances progress to osteoarthritis.

Various animal models have helped us to understand the biology of cartilage repair; however, due to the anatomical and biomechanical differences, they cannot give evidence on the natural history of cartilage defects in humans.

An unanswered issue still remains: do our cartilage repair strategies stop or slow down osteoarthritis process?

At present, only the classical autologous chondrocyte implantation (ACI) technique has a prospective follow-up of over 10 years.

What we know is that the repair tissue does not have the mechanical properties of native hyaline cartilage, leaving the rim of the defect exposed to increased stress. Clinical data with sufficient long-term follow-up regarding different treatment options are not yet available. However, what seems to be the aim of treatment still remains the restoration of the biomechanical environment to near normal.

We can define instability as a shift from the primary load bearing areas to a different location, resulting in overloading of part of the articular cartilage, with a change in both static and dynamic loading with increased stress through the articular cartilage.

The ACL is the most commonly injured knee ligament and it is a primary constraint to anteroposterior joint translation, and isolated lesions are uncommon. Frequently, other ligamentous structures or the menisci are affected, leading to further compromission of joint stability.

However, there is a lack of evidence that anterior cruciate ligament reconstruction or meniscus repair prevents the development of osteoarthritis in the long term. There is evidence of radiographic osteoarthritic changes in 50–80 % of injured knees even after adequate ACL reconstruction [18].

This can be due to a persistent excessive tibial rotation during demanding activity. This is the case of athletes whose return to high functional, demanding sport is allowed by ACL reconstruction.

In conclusion, joint instability or laxity seems to play an important role in the development of early osteoarthritis even though more studies are needed to better understand and justify our everyday handling of ligamentous injuries.