Clearing Up The Confusion Over Posterior Tibial Tendon Dysfunction
Virtually every foot and ankle surgical symposium held in the United States over the past five years has devoted significant sessions to the pathomechanics, surgical and non-surgical treatment of the symptomatic adult flatfoot condition. Unfortunately, the popular name for this condition, posterior tibial tendon dysfunction (PTTD), reinforces a generally accepted notion that a failure of the posterior tibial tendon (PTT) is the primary etiology of the symptomatic adult acquired flatfoot deformity.
However, there has been recent evidence to the contrary that would, at least, caution us about placing total blame on an attenuated or ruptured posterior tibial tendon as the cause of the painful flatfoot condition. The implications of these recent insights are significant to the degree that we must modify surgical and non-surgical treatment plans accordingly.
Early reports linking a relationship between a ruptured PTT and the developmental flatfoot first appeared in the orthopedic literature during the ‘50s. However, these appeared to be rare, isolated cases.
Documentation of a developmental flatfoot deformity in an adult patient population (secondary to rupture of the tibialis posterior tendon) appeared several times in the orthopedic literature during 1982 and 1983 (Mann and Specht, Jahss, Johnson). The first report of this condition in the podiatric literature was published by Fredenburg in the Journal of Foot Surgery in 1983. During the next two decades, a virtual epidemic of painful adult flatfeet (secondary to attenuation or rupture of the PTT) was reported in the medical literature. At the same time, numerous theories were proposed regarding the etiology and pathomechanics of this complex condition.
What The Literature Reveals About Causative Factors Of PTTD
Several investigators (Ghormley, Anzel, Kettlekamp, Downey) have linked PTTD to rheumatoid arthritis. Myerson has found a subgroup of patients with seronegative spondyloarthropathy. Other authors have dispelled any link between collagen vascular disease and PTTD.
An oft-quoted 1992 study from Holmes and Mann found that 52 percent of patients with the adult acquired flatfoot secondary to PTTD had either diabetes mellitus, hypertension or obesity.
In 1984, Mueller categorized posterior tibial tendon ruptures into three etiologic categories: direct injury, pathologic rupture and idiopathic rupture. Seven years later, Mueller proposed a fourth category, “functional rupture,” which would describe patients who didn’t have complete rupture of the posterior tibial tendon.
Clearly, during the past two decades, the majority of authors writing about symptomatic adult acquired flatfoot have described an insidious onset of tendinitis symptoms associated with the PTT that progress to attenuation or “dysfunction” of the tendon, and subsequently lead to complete rupture. During this evolution, they noted the affected foot was undergoing a progressive alignment change that lead to significant flatfoot deformity.
In 1989, Johnson and Strom proposed classifying PTTD into three stages, linking tendon pathology to clinical presentation and radiographic findings. Myerson added a fourth stage later. Currently, this classification system remains the most often quoted system in the literature (see “How To Classify Posterior Tibial Tendon Dysfunction”).
Is The Current Classification Too Broad?
The Johnson and Strom classification attributes the progressive adult acquired flatfoot to gradual attenuation and subsequent rupture of the posterior tibial tendon. However, it ignores other structural changes, specifically ligamentous attenuation, that I will discuss later in this article.
More often than not, these patients will come into your office, already presenting with Stage II of posterior tibial dysfunction. The Stage II category is too broad in that it encompasses the broad range of a flexible flatfoot, beginning with early attenuation and structural change through progressive ligamentous rupture, rearfoot and midfoot collapse, and finally ending in the rigidity which marks Stage III.
In my opinion, there should be subcategories of Stage II, based upon levels of ligamentous attenuation and degree of deformity. Clearly, there are non-operative and operative interventions better suited for “early” Stage II than “late” Stage II conditions.