Thin clubfoot calf – soft tissue problem

A thin calf is undoubtedly one of the distinctive features of a child with clubfoot.
It’s especially noticeable in unilateral cases, where the difference compared to the healthy leg is easy to see. We address the myths surrounding this issue in the article below.

A SOFT PROBLEM

Although the treatment of clubfoot involves repositioning the bones relative to each other, the core issue and pathoanatomy of the deformity are primarily related to the soft tissues of the lower leg and foot. One could say that clubfoot is a “soft problem” — it is essentially a calf disorder that manifests through the foot.

To recall: in congenital clubfoot, certain bones become displaced relative to one another, but the rotation of the calcaneus, cuboid, navicular, and cuneiform bones around the talus is actually a result, not the cause, of the deformity. This rotation occurs because of strong, abnormal pulling by ligaments, tendons, and muscles — they are what Dr. Ponseti called the “deforming force.” This is the key to understanding both the nature of the deformity and the non-surgical Ponseti method, which is innovative yet relatively simple: it reverses the process of abnormal rotation. The problem is not primarily in the bones or cartilage, although they do show morphological changes, but in the imbalance of the soft tissues — ligaments, tendons, joint capsules, and muscles.
These structures play a crucial role in the abnormal anatomy of a clubfoot.

Because of these uneven forces acting on the foot, it turns inward (inversion), causing the heel to become varus (turned inward). The shortening of the plantar and medial muscle groups leads to forefoot adduction — the calcaneus becomes locked under the talus, and the remaining tarsal bones, connected like beads, shift in sequence.
The short Achilles tendon forces the foot into plantar flexion. In this way, a three-dimensional deformity develops — since a change in the position of one bone in the tarsus affects the position of the others. You can read more about this in the article on the PATHOANATOMY OF CLUBFOOT.

THE STICK

When observing a child with congenital clubfoot, one can clearly notice the slenderness of the affected calf. This is especially visible in unilateral cases, where the comparison to the healthy leg makes the difference striking. However, even in bilateral deformities, the calves are visibly thinner than those of typically developing children — and interestingly, even then, the calf volumes can differ from each other. Why does this happen?
Both the clubfoot and the calf on the affected side are characterized by muscle atrophy — a significant reduction in the size and volume of certain muscles — and by fibrosis, meaning an overgrowth of dense connective tissue that replaces normal muscle fibers.

MUSCLE ATRPHY IN CLUBFOOT

In clubfoot, muscle atrophy primarily affects the posterior–medial compartment of the leg, and to a lesser extent, the anterior–lateral compartment. This imbalance appears to be the main cause of muscular disequilibrium, as shown by pathological studies in fetuses and MRI studies in both untreated newborns and treated children
(“Clubfoot pathology in fetus and pathogenesis. A new pathogenetic theory based on pathology, imaging findings and biomechanics – a narrative review,” E. Ippolito, G. Gorgolini*).

The bellies of the gastrocnemius–soleus complex and the tibialis posterior muscle are fibrotic — they are smaller in volume, shorter, and have longer, thickened tendons compared to healthy muscles. In the affected foot and calf, there is less muscle tissue overall, but more fat tissue, which is thicker and located beneath the fascia and within the intermuscular spaces. Some tendons, muscles, and ligaments are also slightly displaced medially, such as the tibialis posterior, extensor digitorum longus, and extensor hallucis longus muscles.

DEFICIT?

Some morphometric studies have shown a predominance of type I fibers and a reduction of type II fibers in the posterior compartment muscles of the leg, along with grouping of type I fibers and clear differences in fiber size. However, more recent research conducted on a large number of samples taken from idiopathic clubfoot muscles in the same compartment demonstrated a normal ratio of type I to type II fibers.

An electromyographic (EMG) study performed on 52 children with congenital clubfoot revealed neurogenic electrophysiological patterns in 83% of cases, mainly affecting the peroneal (fibular) muscles. The authors suggested that idiopathic clubfoot might result from a neurologically based muscular imbalance. However, this hypothesis was not confirmed by subsequent electrophysiological studies of clubfoot muscles.

MYTHS

“The child has a thinner calf because of the cast and treatment.”

This myth is incredibly common — especially among physiotherapists — and we’re here to debunk it. Muscle atrophy is a primary pathology, appearing already in the early stages of fetal development, and it is present in newborns before any treatment begins. Therefore, it is a congenital anomaly, not a result of foot or leg positioning in the womb, nor of treatment such as casting.

There is a hypothesis that muscle atrophy may be linked to the TBX4 and PITX1 genes, which in mice cause muscle atrophy in exactly the same regions of the leg and foot as in humans. You can read more about these findings in our article on the GENETICS OF CLUBFOOT.

Over 80% of children with congenital clubfoot have a poorly developed anterior tibial artery, yet even in such cases, the vascular system functions normally. The veins, arteries, and capillaries continue to supply oxygen to the fibrotic muscles, allowing them to function properly and maintain the limb’s health for many years.

“It will stretch out!”

This is yet another myth, often repeated by physiotherapists (and sometimes even by doctors) about the shortened foot affected by clubfoot. Its shortening is caused by deficiencies and natural contractions within specific muscle groups, tendons, and ligaments, as well as by altered bone and cartilage size and shape. These anomalies develop early in fetal life (as we’ve already mentioned).

There is no way to lengthen the foot through massage, taping, or manual techniques.
In fact, improper manipulation can actually cause harm, because the structure of a clubfoot is fundamentally different from that of a healthy foot — and that difference lies in its anatomy itself.

CAPABLE AND STRONG

Despite the quantitative differences in muscle structure, studies of muscles, nerves, and blood vessels show that the leg musculature on the affected side develops normally and remains efficient and capable of many physical activities.
Many people born with clubfoot go on to become marathon runners, skaters, and athletes.
In Poland, for example, Maciej Lepiato, a Paralympic athlete, was born with this condition.

DON’T WORRY!

A smaller foot (resulting from structural deficits and atrophy) and a slimmer calf will remain with the child for life. It’s estimated that a clubfoot is about 5% shorter (when standing) than a healthy foot — typically a difference of 1 to 1.5 cm. This difference can become much greater if the foot undergoes certain surgical procedures, such as posteromedial release, complete subtalar release, or various types of osteotomy.