Presentació i instruccions.

Osteoarthritis (OA) is the most common type of arthritis with an estimated 15.8 million sufferers in the United States (Pai et al., 1997) and up to one third of 63-94 year olds are living with the condition. It is also the fourth leading cause of non-fatal burden in the world (World Health Organisation, 2002). The knee is the most common joint associated with the disease (Sharma et al., 1997). Unfortunately for sufferers there are a number of debilitating effects of OA. Structural changes cause an increase in the regional load across articular cartilage in the joint and this negatively influences the material properties of the tissue and hence reduce the joint’s ability to withstand load (Pai et al., 1997). There is often reduced stability in the knee of OA sufferers potentially caused by changes in the bony geometry, muscular contraction patterns and ligament and capsule deficiencies in and around the joint (Pai et al., 1997). As anatomy of the knee changes with OA progression and this is thought to reduce proprioceptive ability, research has considered the effect of OA on knee proprioception using both JPS and TTDPM techniques.

Research strongly suggests patients with OA have an increased threshold to detect passive motion (Pai et al., 1997, Sharma et al., 1997, Koralewicz and Engh, 2000, Collier et al., 2004, Lund et al., 2008, Hewitt et al., 2002, van der Esch et al., 2007, 2013, Cammarata et al., 2011, Chang et al., 2014, Sanchez-Ramirez et al., 2013). The severity of OA in these patients ranged from grade 1 to grade 4 (Kellgren/ Lawrence grading). Most studies used either a custom built machine or an IKD to collect flexion and/ or extension TTDPM data. However, Chang et al., (2014) considered valgus / varus movement. All studies used aged matched controls. Interestingly, studies that also included comparisons to the contralateral knee in OA patients reported a reduced TTDPM ability compared to external controls and no significant difference compared to the OA knee (Sharma et al., 1997). This suggests the undiagnosed knee may also have proprioceptive impairments.

As well as differences between groups, studies also considered the relationship between kinaesthesia sensibility and other OA characteristics. For example, Cammarata et al., (2011) Hewitt et al., (2002) and van der Esch et al., (2007)found no correlation between TTDPM measures and stiffness, age, gender, pain or WOMAC (Western Ontario and McMaster

Universities Arthritis Index) scores. Koralewicz and Engh, (2000) found no relationship between severity of OA (measured by radiography) and TTDPM ability. However van der Esch

et al., (2013) did find an inverse relationship between number of lesions in the knee of OA patients and TTDPM; that is as the number of lesions increased, kinaesthetic sense decreased. Furthermore TTDPM ability has been linked to functional tests such as single leg balance (Sanchez-Ramires et al., 2013), activity levels (Holla et al., 2012) and walking times (van der Esch et al., 2007). The relationship between TTDPM and function was stronger if muscle strength was added to the regression model (van der Esch et al., 2007).

Studies have also considered the effect of OA on knee JPS (Garsden and Bullock-Saxton, 1999, Hurley et al., 1997, Mohammadi et al., 2008, Bayramoglu et al., 2007, Marks et al., 1993, Barrett et al., 1991b, Hassan et al., 2001, Bennell et al., 2003, Hall et al., 2006, Segal et al., 2010, Felson et al., 2000, Sanchez-Ramirez et al., 2013). All JPS protocols involved target and reproduction angles. However, there are many differences in other measurement variables such as weight bearing / non weight bearing conditions (for example Marks et al., 1993), matching methods (for example visual analogue scale in Barrett et al., 1991b) or active matching (Marks

et al., 1993, Hall, 2006), equipment (for example electrogoniometery in Mohammadi et al., 2008) or IKD (Bayramogku et al., 2007). However, this variability did not appear to influence findings; the majority of research indicated patients with OA have reduced JPS ability. However Hall et al., (2006), Lund et al., (2008) and Bayramogku et al., (2007) did not find a difference in JPS between OA patients and age matched controls. They attributed this finding to a potential degeneration of the elderly control knees without diagnosis, lack of severe grade OA patients in the sample or lack of sensitivity of the measurement tool. Alternatively, it may be that JPS does not reduce with OA and the reduction in JPS ability preceded the disease (Lund et al., 2008).

The effect of OA on JPS was also considered using regression analyses. There were no relationships between JPS ability and pain, clinical scores or walking speed, (Marks et al., 1993, Bennell et al., 2003). Indeed Hassan et al., (2001) concluded the most significant predictors of OA progression were BMI and maximum voluntary quadriceps contraction. This is supported by Segal et al., (2010) who concluded knee JPS is not a valid predictor of OA condition alone. However, Felson et al., (2000) did find correlations between JPS and pain and WOMAC scores in OA patients that is as JPS ability got worse, so did pain and WOMAC scores across a 30 month period. It must be noted correlation analysis alone cannot provide

cause and effect and regression analysis only explains a certain amount of variance in the data, therefore findings must be generalised with caution.

It may be joint effusion of OA knees that prevents optimal JPS performance. However, there is only limited evidence to support this. McNair et al., (1995) considered the effects of injected saline into uninjured knees and concluded the artificial effusion did not reduce JPS ability. ConverselyCho et al., (2011) concluded OA patients injected with saline did have reduced JPS ability, but only is non-weight bearing conditions. Therefore it is still unclear what effects, if any, joint effusion has on proprioception.

Unfortunately, there are many negative consequences of OA. These include tenderness, limited range of motion, effusion or inflammation and most commonly, sustained joint pain (Kaya, 2014). Radiographic analysis of the pathological joint can further reveal asymmetric joint space narrowing, cyst formation, osteophyte formation and subluxation effects of the disease (Kaya, 2014). It is suggested the three consequences most likely to influence proprioception ability are impaired articular mechanoreceptors and hence modulated afferent discharge, muscle weakness that reduces gamma motor neurone activation and muscle sensitivity, inflammation / effusion and injuries to other structures in the joint such as meniscus (Knoop et al., 2011). These variables may all contribute to modifying the articular afferent discharge and hence joint proprioception which in turn may reduce function. However the research discussed is that of retrospective design and it cannot be deduced if the disease caused the proprioceptive design or poor proprioceptive ability preceded the onset of OA. OA progression certainly has a linear relationship to degeneration of the articular tissues, hence it would follow articular mechanoreceptors would be damaged and afferent signals would be modulated (Lund et al., 2008). This may reduce the sensitivity of the gamma motor neurones and then proprioception. On the other hand there is some evidence to suggest patients with OA may have had decreased proprioceptive ability prior to the disease diagnosis (Cammarata et al., 2011). Indeed contralateral knees and upper limb joints of OA patients have been shown to have decreased proprioceptive ability compared to uninjured matched controls (Sharma et al., 1997, Lund et al., 2008). Furthermore, it is thought up to a third of women with unilateral OA will have bilateral OA within two years of diagnosis (Garsden and Bullock-Saxton, 1999) and there is up to a 90% contralateral OA risk within 10 years (Jones et al., 2013). Despite these theories, a recent narrative review on proprioception and OA (Knoop et al., 2011) could not find any clear evidence to link impaired mechanoreceptors, reduced muscular strength and hence reduction in spindle sensitivity or inflammation in OA patients to the decline in joint

proprioception. There has been some correlation analysis on proprioceptive ability and decreased functional ability; however the evidence is far from extensive.

Whether the disease is in fact the cause or effect of reduced proprioception will need to be considered in more detail using longitudinal study designs in future research. However, importantly and in continuation of other sections in this literature review, the methodologies used to collect joint position sense and threshold to detect passive motion data were inconsistent; a wide range of equipment, angular displacements, angular velocities and angular directions were used to name but a few of the method variables. Importantly studies also found patients with OA were not always able to complete fully weight bearing testing. Therefore it is important a standardised method is identified to measure knee proprioception before these longitudinal studies can take place. There was also a lack of normative data on either knee joint position sense or threshold to detect passive motion.