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This quarterly column from the AAOS Women’s Health Issues Advisory Board and the Ruth Jackson Orthopaedic Society provides important information for your practice about issues related to sex (determined by our chromosomes) and gender (how we present ourselves as male or female, which can be influenced by environment, families and peers, and social institutions). It is our mission to promote the philosophy that male and female patients experience and react to musculoskeletal conditions differently; when it comes to patient care, surgeons should not have a one-size-fits-all mentality.

AAOS Now

Published 3/1/2003
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Laura Gehrig, MD

Posterior tibial tendon dysfunction: More prevalent in women

By Laura Gehrig, MD

“My foot hurts and my arch has collapsed. I can’t wear the shoes I want to anymore.”

Many orthopaedists have female patients with similar foot complaints. Although some orthopaedists may not appreciate the significance of limited shoe style options, it is problematic for many women. Moreover, these patients want to feel better. So what is the science behind “fallen arches” and why are more women than men affected?

Symptomatic flatfoot: AAFD/PTTD
Flatfoot does not have to be painful. Historical research indicates that some primitive peoples in Africa and Australia were all flatfooted. Although many adults have asymptomatic flatfoot, the symptomatic flatfoot that develops over time and is brought to the attention of orthopaedists is known as adult acquired flatfoot deformity (AAFD) or posterior tibial tendon dysfunction (PTTD).

PTTD encompasses a spectrum of pathologic changes that progressively affect the posterior tibial tendon. These changes, depending on severity (stages I-IV), manifest as various alterations in foot and ankle tissue and, subsequently, kinematics. Strength and function change during gait patterns as the tendon and ligaments become weak. Swelling and pain may lead to deformity and changes in the shape of the foot. Disability, difficulty with shoe wear, and altered gait can result. In the later stages of the disease (stages III and IV), standing or walking can be painful.

Ligament changes in the foot in PTTD are not isolated to the posterior tibial tendon. The ligaments of the foot that undergo the most severe changes and degenerative involvement in patients with PTTD are the spring ligament complex (superomedial and inferomedial calcaneonavicular) and the talocalcaneal interosseous ligament, with the spring ligament being most affected. Ligament pathology is nearly as common as posterior tibial tendinopathy, and the goal of treatment should therefore be to prevent progressive failure of these structures.

Etiology of PTTD
Why does the PTT degenerate? The etiology is unclear. What is known is that patient factors do play a role. More than half of all patients with a ruptured PTT also have a history of hypertension, obesity, diabetes, a previous operation or trauma about the medial aspect of the ankle, or treatment with steroids. Hypovascularity of the tendon, previously believed to play a role, has been excluded as an etiologic factor based on a cadaveric study in which vascularity of the tendon did not differ with respect to patient age, sex, or side.

Changes in collagen may influence the development of PTTD. Injury and inflammation may weaken collagen tissue. Moreover, normal adult collagen undergoes very little metabolic turnover. Hence, fibrotic tissue and scar may be deposited in the tendon. After surgery or trauma, the deposition of collagen fibrils (scar) during the repair process is largely irreversible and is a major feature of the pathologic changes.

An alteration in collagen content is also associated with PTTD. In a small study of nine patients with PTTD, damaged tissue had a higher proportion of type II collagen and relatively less type I collagen than normal tendon tissue. The analysis of results made no distinction between males and females. The authors concluded that the degenerative process results from marked changes in not only molecular composition of matrix collagens but also in structural organization. This change in composition would likely alter the mechanical resistance of the tissue, allowing kinematic changes to occur.

PTTD: More common in women
Recent literature has reported a higher prevalence of PTTD in women than in men, but with no explanation for this discrepancy as yet. Because the condition in women peaks during perimenopause, hormonal influence may have a role in degeneration of the tendon. The same processes that affect changes in bone (collagen I) during menopause could also affect tendons and ligaments, thereby contributing to the increased incidence of PTTD in women in their 50s.

Conclusion
It is not understood why PTTD is more prevalent in women than in men. Although comorbidities such as diabetes and obesity and mechanical influences such as trauma to the medial ankle have been reported to contribute to PTTD, they have not been analyzed based on sex. Likewise, pathologic changes in the tendon and ligaments at the structural level have been documented but without sex analysis. Because the prevalence of PTTD in women peaks during perimenopause, hormonal influence from loss of estrogen may be postulated as a factor in the prevalence of PTTD in women.

Elucidating the reasons for the discrepancy in the prevalence of PTTD between men and women will require further research into the role of changes in collagen matrix composition with aging, hormonal influences, and injury patterns in men and women.

References for the studies and statistics cited in this article can be found in the online version, available at www.aaosnow.org

Laura Gehrig, MD, is a member of the AAOS Women’s Health Issues Advisory Board. She can be reached at laura.gehrig@gmail.com

Putting Sex in Your Orthopaedic Practice

References:

  1. Mann, Roger A. Chapter 10 Miscellaneous afflictions of the foot, Surgery of the Foot . The C.V. Mosby Co., St. Louis 1986, page 230.
  2. Myerson, Mark S., MD., Baltimore Maryland Instructional Course Lectures, The American Academy of Orthopaedic Surgeons –Adult Acquired Flatfoot Deformity. Treatment of Dysfunction of the Posterior Tibial Tendon, JBJS (American). 1996;78:780-792.
  3. Deland JT, de Asla RJ, Sung IH, Ernberg LA, Potter HG. Posterior tibial tendon insufficiency: which ligaments are involved? Foot Ankle Int. 2005:26(6):427-435.
  4. Holmes, G.B. Jr., and Mann, R. A.. Possible epidemiological factors associated with rupture of the posterior tibial tendon. Foot and Ankle. 1992;13:70-79.
  5. Prado MP, de Carvalho AE, Rodrigues CJ, Fernandes TD, Mendes AA, Saloao O. Vascular density of the posterior tibial tendon: a cadaver study. Foot Ankle Int. 2006; 27(8):628-631.
  6. Braunwald, Eugene, Fauci Anthony S, Kasper Dennis L, Hauser Stephen L, Longo Dan L, Jameson J, and Harrison Larry. Principles of Internal Medicine, ed. 15. New York; McGraw-Hill; 2001, pp. 2290-2292
  7. Gonçalves-Neto J, Witzel SS, Teodoro WR, Carvalho-Júnior AE, Fernandes TD, Yoshinari HH. Changes in collagen matrix composition in human posterior tibial tendon dysfunction. Joint Bone Spine. 2002 Mar;69(2):189-194.