The retinacula of the ankle has classically been considered as an autonomous organ that plays a key role in a pulley system including the peroneals, flexors, and extensors surrounding the ankle, however, this may not be the retinacula’s reality.
In 1984, Antonio Viladot and colleagues evaluated the embryology and ontology of the subtalar joint’s function including anatomical and histological assessment of the retinacula. The authors determined that the retinacula consisted of three parts including areas invested with striated muscle tissue of the plantar intrinsics and some flexors and extensors of the ankle joint. Additionally, the retinacula demonstrated a high preponderance of neural structures that are sensory in nature contained within a lax, elastic tissue, particularly in the lateral aspect.
Carla Stecco and colleagues more recently have explored the anatomy and histology of the retinacula that also begets a number of questions. The researchers discovered that the retinacula is discernible but not separable from the crural fascia and has a number of different orientations and thicknesses. The tissue contained a large volume of type I and II mechanoreceptors including Golgi organs, Ruffini, and Pacini organs demonstrating similar continuity of muscular tissues and periosteum. Stecco also noted that the tissue was somewhat and smaller percentage of collagen formation that were variable in areas. Biedert and colleagues also noted a great deal of interstitial type III and IV mechanoreceptors within the retinacula (1992).
The elastic nature of the tissue requires reconsideration of the retinacula’s role in mechanical stability and the interdigitation of muscular tissue and high presence of sensory neurons suggest it may have a role in reflex motor activity and proprioception. As the retinacula is distinguishible but inseparable from the crural fascia, the area may best be considered a functional specialization of fascia.
Role of Retinacula in Ankle Instability
Chronic ankle instability (CAI) is a problematic sequelae to ankle sprain in a fairly sizable amount of the population (~30-40%) that presents with repeated injury and reinjury, reduced joint position sense, greater postural sway, and changes in muscle activation.
Ten of 17 subjects in Stecco’s research with a previous lateral ankle injury demonstrated retinacular abnormalities including thickness and full-gap separations from the periosteum as measured by MR imaging. This loss of direct continuity with the periosteum and muscular tissues may be part of the articular deafferentation and reflex latency picture so common following lateral ankle injury and predisposing individuals to chronic ankle instability.
We are well aware that interfascial mechanoreceptor stimulation can modulate gamma motor neuron activity responsible for postural organization and anti-gravity extensor activity, all of which are disturbed in CAI (Bullock-Saxton, 1994; Glaser, 1980; Schleip, 2003). Interstitial mechanoreceptors have also been associated with joint position sense, which, too, is disturbed in ankle dysfunction.
It has also been recently demonstrated that plantar intrinsics demonstrate a reduction in activity as measured by navicular drop in single leg stance (Drewes, 2008). In Drewes’s study, those in the CAI group demonstrated poor performance 61% of the time compared to 28% in the healthy controls. Peroneal activation, which is reflexively stimulated by supination and stretch of the lateral aspect of the retinacula (Viladot, 1984), is also delayed in CAI.
Not Just a Local Phenomenon
The impact of deafferentation also results in motor consequences at the hip and core and CAI subjects often complain of low back pain (Marshall, 2009).
Bullock-Saxton (1994) noted delayed onset function of the gluteus maximus and Beckman (1995) noted changes in hip abductor function following ankle injury. This dysfunction in the motor system is likely a result of dysfunctional afferent-efferent coupling that influences the quality of muscular response to perturbation. Because the retinacular mechanoreceptors are unable to respond appropriately, appropriate motor response may not occur in antigravity tissues.
Dr. Liebenson also notes that changes in positions ultimately can lead to further dysfunction in the plantar intrinsics, creating a vicious circle.
Stecco and colleagues suggest, too, that ankle injuries do not have to occur for this proprioceptive deficit to occur because of the continuity of the crural fascia. Anything that places adverse tension upon the crural fascia can result in propriceptive dysfunction and potentially lead to altered motor responses. Additionally, any excessive motion about the ankle may lead to increased collagen activity, retinacular thicknesses, and a possible negative influence on the sensory function.
Based on the interdigitation of muscular tissues and the density of mechanoreceports, the role of retinacula is far more than a simple mechanical component of a pulley system. In the coming weeks we’ll address the sensory nature of various fascial organs and how they are influenced in greater detail.