Foot pain and deformities are commonly encountered in patients with rheumatoid arthritis (RA). Likewise, Posterior tibial tendon dysfunction (PTTD) is commonly involved in development of foot and ankle abnormalities and has been reported with a prevalence in two-thirds of the RA patients.
Redundancy in the physiological function between different muscles provides the central nervous system multiple options to perform the same movement but which muscles compensate for the impairment of the tibialis posterior (TP) muscle? And how does these changes affect ankle joint loading?
Experimental and computational disciplines were applied to investigate changes in muscle forces as result of induced pain in the right TP muscle. Twelve healthy subjects were enrolled in the study. Experimental pain was induced in the TP by a single ultrasound graphically guided injection of 1â€¯mL hypertonic saline (5.0% Sodium Chloride). The participantsâ€™ gait was assessed by skin marker-based motion capture and force plates. Musculoskeletal models were used to investigate compensation mechanisms systematically in the lower under extremity when TP muscle was recruited less as a consequence of the induced pain.
Experimental TP muscle pain and simulated reduced strength caused altered muscle recruitment and made the flexor digitorum longus and flexor hallucis longus muscles compensated for the impairment of the TP muscle. Further, the resultant ankle joint force was increased as the strength of the TP muscle was reduced.
The compensation mechanism observed in the present study indicate that alterations in muscle recruitment and muscle force distribution as a result of the underlying disease inflammation itself may contribute to development of chronic foot pain and deformities in patients with RA. Further studies are required to understand the role of PTTD in occurrence of those late adverse musculoskeletal manifestations aiming at search for early preventive strategies.