Hello everyone,
I would just like to add a few comments to the tib. post dysfunction
discussion. Firstly has anyone read the article by Hodges Davis and
co-workers (1996) regarding the spring ligament? They found that there are
two components to the spring ligament: the superomedial calcaneonavicular
ligament and the inferior calcaneonavicular ligament. Importantly, the
histological properties of the supermedial ligament had significant
load-bearing properties, with an articular facet that helped "sling" or
support the talar head. This highlights the importance of this ligament in
maintaining the arch of the foot by resisting talar plantarflexion. In
addition, the ligament in all 38 cadavers had direct attachments to the
tibialis posterior tendon and the deltoid ligament which further
demonstrates the link that each structure has with the others.
Consequently, if one goes, it would be difficult for the others to
maintain integrity. Although I invariably forget about the deltoid
ligament when dealing with tib. post. dysfunction, it has been recognised
by Jahss (1991) for some time now that the distal tibia is subjected to
spurring (ie. due to tension at the proximal portion of the deltoid
ligament) as the tib. post. tendon lengthens and the arch flattens.
Clearly, it 'cops a hiding' in this condition too.
Finally, we need to be careful to not only focus on biomechanics when
discussing tib. post. dysfunction. If this condition was only caused by
excessive pronation, we would no doubt see more cases of it. Holmes and
Mann (1992) found from their epidemiological study that all subjects in
their series had one of the following (i) hypertension, (ii) obesity, (iii)
diabetes mellitus, (iv) previous surgery or trauma about the medial aspect
of the foot, or (v) steroid exposure. Further, there was a statistical
correlation between rupture of the tib. post. tendon and hypertension and
obesity. These factors may all interrupt the blood supply to the tendon,
especially in the 'zone of transition' as described by Frey et al (1990).
The 'zone of transition' is an area, similar to that in the Achilles
tendon, where there is a poor blood supply, and not surprisingly, this
corresponds to the site at which dysfunction and rupture occur. Although
excessive pronation will place extra stress on this area, it may only be
one of a number of abnormalities that may.
References:
Frey C, Shereff M & Greenidge N. (1990) Vascularity of the Posterior
Tibial Tendon. J. Bone & Joint Surg. 72A: 884-888.
Hodges Davis W, Sobel M, DiCarlo EF, et al. (1996) Gross, Histological,
and Microvascular Anatomy and Biomechanical Testing of the Spring Ligament
Complex. Foot and Ankle Int. 17(2): 95-102.
Holmes GB & Mann RA. (1992) Possible Epidemiological Factors Associated
with Rupture of the Posterior Tibial Tendon. Foot & Ankle 13: 70-79.
Jahss MH. (1991). Tendon Disorders of the Foot and Ankle. In MH Jahss
(Ed.), Disorders of the Foot and Ankle (2nd ed.). (pp 1461-1513).
Philadelphia: W.B. Saunders.
Cheers,
Karl Landorf
Lecturer
Division of Podiatry
Faculty of Health
University of Western Sydney, Macarthur
P.O. Box 555
Campbelltown NSW 2560
AUSTRALIA
Phone: (02) 4620 3758
Fax: (02) 4620 3792
Website: http://FOHWEB.macarthur.uws.edu.au/podiatry/welcome.htm
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