The term patellar instability has been used in different contexts in the literature including abnormal tilting or positioning of the patella [36, 37] but is here used to describe persistent maltracking which is associated with episodes of symptomatic subluxation or dislocation. Instability and malalignment of the patellofemoral joint are major causes of knee symptoms in young people [20, 22, 38].

In full extension, the patella lies above the trochlea, and it is in early flexion that it articulates first at the distal pole and facets. As flexion progresses, contact occurs more proximally on the patella (and distally on the trochlea). Therefore, the contact surfaces and pressure on patellar facets changes throughout the range of motion, increasing the stabilising forces through the range of knee flexion [39].

Stability is provided by both bony and soft tissue stabilisers [8] and correlates with the geometry of the distal femur [40]. In the clinical evaluation of patellar tracking, it has been recommended that the patella is observed as it enters the femoral trochlear groove. In normal tracking, the patella moves smoothly into the femoral trochlea during initiation of flexion, and in terminal extension, there is minimal lateral displacement seen as the patella leaves the trochlea and occupies a supracondylar position. Exaggeration of this normal motion can be seen subjectively during clinical examination in the J-sign during initiation of flexion in patients with instability (see Chap. 1). This refers to the inverted “J” course of a patella that begins lateral to the trochlea then moves suddenly medially to enter the trochlea [41]. Although other patellofemoral pathological signs can be common in asymptomatic knees, the J-sign is almost universally associated with pathology [42]. A strong correlation has also been demonstrated between the presence of patellar tilt during clinical examination and tilt seen on magnetic resonance imaging (MRI) scans, such that patients with significant tilt on the physical examination can be expected to have an MRI tilt of 10° or greater whereas an angle of less than 10° is associated with the absence of significant tilt on the physical examination [38].

The first line of treatment of patellofemoral instability involves physiotherapy with strengthening of the quadriceps focusing on the VMO, although it is debatable whether this can be selectively isolated in practice [64, 65]. For patients without overt dysplasia, physiotherapy remains a good option [66] and newer techniques, such as biofeedback, can improve the results [67].

Lateral patellar dislocation is associated with MPFL rupture in 87–100 % of patients [36, 68–70] and in the longer term, patellar instability and dislocation are associated with chondral injury and osteoarthritis [69, 71]. Non-operative management may leave a third of patients with significant symptoms, two fifths with at least one episode of further dislocation and half unable to return to vigorous sports at long-term follow-up [70]. Surgery can correct recurrent dislocation which without treatment can occur in 42–49 % of patients [70, 72].

Surgical treatment must depend on the primary pathology and identification of this pathology is mandatory for successful treatment of instability. Repair or reconstruction of the MPFL is indicated when soft tissues rather than bony morphology are the primary pathological feature [73–77]. Tibial tubercle advancement transfer [53, 78–80] or sulcus deepening trochleoplasty [81, 82] are considered favourable treatments for pathoanatomy such as increased tibial tubercle to trochlear groove (TT-TG) distance or trochlear dysplasia respectively [83, 84]. Guided growth for deformity correction has been described [85] as instability can present prior to skeletal maturity although some surgeons will elect to wait until physes have closed to avoid complications such as growth arrest [86]. An isolated lateral ligamentous release will only work for a proportion of patients and has not shown as favourable results as the other options above [87] because it cannot alone resolve all of the causative factors listed. Further research is necessary to understand the best surgical treatment for patellar dislocation. A Cochrane review found only poor quality evidence supporting any surgical treatment for patellar instability, with no trials examining people with recurrent dislocations, which are those most likely to require surgical management [88].

Patellofemoral osteochondral defects can be associated with osteochondral or bone marrow lesions on imaging studies. MRI can be used to detect bone oedema even in the absence of fracture or defect on plain radiographs. OCD may be the precursor to patellofemoral arthritis although further research is required to determine the risk factors for progression to OA [89, 90]. Osteochondral injuries are associated with patellar instability and dislocation [91–93]. This is important as missed or delayed diagnosis can lead to chronic pain, decrease in sports, social and working activities, with the associated socioeconomic impact, even when the primary pathology leading to the instability is addressed.

Before the OCD itself can be treated, firstly the stability of the patellofemoral joint must be restored. As mentioned in the previous section, the medial retinaculum is injured with rupture in nearly all patellar dislocations [94] and this will impact the ongoing patellar stability and will compromise any reparative techniques for the cartilage.

Cartilage lesions are described in detail in Chap. 11. Compared to the tibiofemoral joint, and in particular to lesions in the femoral condyles, the shear forces encountered at the patellofemoral joint often render traditional reparative strategies, such as microfracture, unsuccessful. Modern techniques such as stem cell or chondrocyte implantation are showing promising early results [95] and matrix-induced autologous chondrocyte implantation (MACI) may offer an alternative solution in experienced hands [96, 97]. With ongoing technological progress, the high costs of such procedures may continue their downward trend but in areas of larger cartilage defects there are proponents for alternatives such as inlay arthroplasty [98] or osteochondral allograft transfer [99].

Isolated symptomatic patellofemoral osteoarthritis has been reported in 2 % of men and 8 % of women older than the age of 55 [100] and a prevalence of 9 % was noted in a series of 174 patients presenting to an orthopaedic a single centre with knee pain [101]. The aetiology of patellofemoral joint (PFJ) OA can be divided into surface pathomorphology and soft tissue imbalance. Evidence of trochlea dysplasia has been shown in 78 % of knees with isolated patellofemoral arthritis [102, 103]. The same factors implicated in patellar instability can predispose to OA: the extensor mechanism can be affected by excessive Q-angle [104], patella alta and tibial tubercle malposition [105]. A laterally positioned tibial tubercle [106, 107] and valgus alignment have been associated with PFJ OA [20, 107–109].

Physiotherapy to strengthen the quadriceps muscles has been shown to be beneficial [110]. Lifestyle measures including activity modification and weight loss should also be considered key parts of treatment, particularly for patients with malalignment [111].

Surgical treatments include tibial tubercle elevation, total knee arthroplasty and patellectomy [112–114] although the latter has been much debated [115] and has now largely fallen from favour due to associated loss of extension power [116]. Newer options such as chondrocyte implantation are also being used in PFJ OA [117] although this is a developing field with only early results.

Arthroplasty interventions are beyond the scope of this book but will be dealt with briefly. Total knee arthroplasty (TKA) has had good results although it requires more soft tissue releases for isolated PFJ OA compared to tricompartmental knee OA [112]. One of the main issues with the patellofemoral articulation in TKA may be the design of the trochlear groove [118]. Patellofemoral joint replacement is a bone preserving procedure [119] and has gained popularity in treating isolated PF osteoarthritis in young patients [120–123]. Although early designs suffered from higher revision rates of up to one third, this has now improved dramatically [124], with some surgeons reporting no revisions at 5 years follow-up in a group of 50 patients [125]. The most common cause for revision was progression of tibiofemoral arthritis [126] although significantly less frequently when the patellofemoral arthritis had been secondary to femoral trochlear dysplasia [127]. Patient selection is of paramount importance and younger patients, those with dysplasia or previous patellofemoral trauma are the most suitable candidates as opposed to those with idiopathic arthritis or disease in other compartments [119, 128]. Patellofemoral joint replacement is a complex procedure as not only is the pathomorphology varied as discussed above but also placing even a well designed prosthesis correctly is challenging. Most femoral implant designs show characteristics of trochlear dysplasia [129, 130] and traditional surgical instruments allow significant variability in implant positioning. Patient-specific implants [131] and computer-assisted patellofemoral arthroplasty with preoperative planning [132] may improve component placement and accurate restoration of joint surfaces.