The pathology, the functional anatomy of clubfoot and the structural changes in its ligaments, tendon, and muscles, must be well understood to arrive at a smart approach to early non-surgical treatment this of deformity.
THE BASE OF UNDERSTANDING
To fully understand the pathology of the clubfoot, it is essential to understand the ANATOMY of the healthy foot, free of any anomalies. This serves as the foundation, and without this knowledge, it is impossible to fully grasp the pathoanatomy, or the disrupted structure.
The structure of the ACHILLES TENDON is the second crucial element that cannot be overlooked, as it is problematic in children with clubfoot.
It is important to remember that clubfoot is a three-dimensional deformity, meaning that the specific “directions” of this pathology, which are closely related to FOOT MOVEMENTS, must be systematically categorized. Experience shows that understanding the independent movements of the foot is one of the most challenging and time-consuming concepts to grasp. However, this knowledge is essential, as it establishes a systematic framework used in orthopedics.
HISTORICAL DISCUSSION
The pathology of congenital clubfoot has intrigued scientists for centuries. The non-specific nature of the condition causes researchers to not only try to answer the question: where does this defect come from, but also what is the problem associated with it?
Clubfoot was well described in 1803 by the Italian anatomist and professor Antonio Scarpa in his work "Memoria chirurgica sui piedi torti congeniti." Scarpa observed that the navicular, cuboid, and calcaneus bones were medially displaced and rotated in relation to the talus. At the same time, he believed that the abnormalities of the muscles, tendons, and ligaments of the foot and leg were secondary deformities resulting from the bone deformities. However, it was only Dr. Ignacio Ponseti, together with Dr. Ernesto Ippolito from Italy, starting in 1947, who extensively studied the anatomical and histological aspects of many deformed feet, as well as healthy feet from aborted fetuses (abortions between 16 and 24 weeks of pregnancy), stillborn children, and those who died shortly after birth. Thanks to their work, we now have a better understanding of the structure and pathology of such a foot.
"SOFT" PROBLEM
In congenital clubfoot, certain bones are displaced relative to each other, but the rotation of the calcaneus, cuboid, navicular, and cuneiform bones around the talus is a consequence, not the cause, of the deformity. This rotation is caused by the very strong pulling of ligaments, tendons, and muscles – they possess the "deforming power." This is the key to understanding the problem of the defect itself and its non-surgical treatment method, which is highly innovative, yet relatively simple, and involves reversing the rotational process.
The problem is not the pathological structure of the bones and cartilage (although morphological changes do occur here) or their arrangement, even though that is how it manifests, but rather the imbalance that occurs in the soft tissues: ligaments, tendons, joint capsules, and muscles. This imbalance is one of the key aspects of the pathological structure of the clubfoot. It is primarily a calf condition that manifests... in the foot.
As a result of these uneven forces acting on the foot, it is positioned in inversion, causing the heel to become varus. The shortening of the plantar and medial muscle parts leads to the adduction of the forefoot – the calcaneus blocks beneath the talus, and the remaining bones, like beads connected together, shift. The shortened Achilles tendon positions the foot in plantar flexion. In this way, a three-dimensional deformity develops, as the displacement of one of the tarsal bones affects the position of the others.
MUSCULAR ATROPHY
When observing a child with congenital clubfoot, a noticeable thinning of the calf is seen. This is particularly evident in children where the defect affects only one foot (and correspondingly, one calf). However, even in children with a bilateral deformity, the calves are noticeably slimmer compared to the "standard" and healthy children's calves. Interestingly, even with bilateral deformity, the volume of the calves can differ from each other. Why does this happen? The clubfoot and the calf on the affected side are characterized by muscular atrophy, which means a significant reduction in the volume and size of certain muscles, and fibrosis, which refers to the overgrowth of connective tissue with a regular and compact structure that is more abundant than the muscle tissue.
Muscular atrophy in clubfoot primarily affects the muscles of the posterior-medial compartment and to a lesser extent the anterior-lateral compartment of the leg. This seems to be the cause of the muscular imbalance, as demonstrated by both pathological studies in fetuses and MRI studies in untreated newborns and treated children.
The bellies of the triceps surae and posterior tibial muscles are fibrotic: they are smaller in volume, shorter, and their tendons are longer and thickened (compared to healthy muscles). In the affected foot and calf, there is actually less muscle tissue but more fat tissue, which is thicker and present beneath the fascia, in the interstitial spaces of the muscles. This is clearly illustrated by an MRI image. Both in the black-and-white and color images on the left, we see a patient with clubfoot. Some tendons, muscles, and ligaments are slightly shifted medially, such as the posterior tibial muscle, long toe extensor, or long hallux extensor. The more advanced the deformity, the greater the calf thinning, as it is affected by more atrophy and fibrosis.
Recent studies conducted on a large number of samples taken from idiopathic clubfoot from the same leg compartments have also shown a normal ratio of type I to type II muscle fibers.
BONE DISPLACEMENTS
Due to the uneven functioning of muscles and other soft tissues, numerous changes occur in the alignment of the bones. Often, these bones, which are very soft and susceptible to deformation, slightly change their shape or become a bit smaller compared to a normal, healthy foot as a result of the displacements.
Following the displaced bones, one can notice that:
The calcaneus (green color) becomes blocked under the talus. The shortened Achilles tendon pulls the back of the blocked bone upward, causing the heel to assume a equine position. As a result, the calcaneus is very difficult to palpate beneath the fat pad. This positioning of the calcaneus results in a strong plantar flexion at the upper ankle joint. The tilting of the calcaneus around the talus (red color) gives the heel a varus alignment relative to the vertical axis of the talus, and its entrapment beneath the talus causes it to be adducted. The shape and size of the calcaneus are also slightly altered.
The talus bone (red color) is also in plantar flexion. Additionally, it is rotated inward, and its lateral part is not covered by the navicular bone – the head of the talus and its exposed edge can be palpated on the lateral side of the foot. The talus is smaller than in a healthy foot, and its head has a wedge-like shape. Sometimes, the entire talus bone is slightly flattened. Just below the head of the talus lies the calcaneus – often, one bone can be mistaken for the other. The head of the talus in a child measures only 0.5 cm in size.
Adduction of the foot is caused by the displacement of the navicular bone (yellow color) onto the medial surface of the head of the talus. The navicular bone then forms a joint only with the medial part of the talar head, which often leads the navicular to come into contact with the medial malleolus. Sometimes, this bone is slightly flattened and has a wedge-like shape on the outer side. The cuboid bone (orange color) moves medially relative to the anterior process of the calcaneus and becomes lowered. The three cuneiform bones (blue color) move downward, aligning medially with the navicular bone. The metatarsal bones are in plantar flexion and adduction, giving the appearance that the foot is "broken" in half.
- Ponseti I.V.: „Congenital Clubfoot. Fundamentals of treatment.” (2nd edition)
- Ponseti I.V., Campos J.: "Observations on Pathogenesis and Treatment of Congenital Clubfoot."
- Gradek J. et al..: "Leczenie wrodzonej stopy końsko-szpotawej metodą Ponsetiego z wczesnym zastosowaniem opatrunków gipsowych – doświadczenia własne."
- Windisch G. et al.: "A model for clubfoot based on micro‐CT data."
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- Ippolito E. et al.: "Leg muscle atrophy in idiopathic congenital clubfoot: is it primitive or acquired?"
- Ippolito E., Gorgolini G.: "Clubfoot pathology in fetus and pathogenesis. A new pathogenetic theory based on pathology, imaging findings and biomechanics-a narrative review."
- Gosztonyi G. et al.: "Morphometric study of muscle in congenital idiopathic club foot."
- Isaacs H. i inni: "The muscles in clubfoot - a histological, histochemical and electron microscopic study."
- Gray D.H. et al.: "A histochemical study of muscle in clubfoot."
- Bohner-Beke A. et al.: "Lower leg atrophy in congenital talipes equinovarus."
- Fulton Z. et al.: "Calf circumference discrepancies in patients with unilateral clubfoot: Ponseti versus surgical release."
- Kerling A. et al.: "The congenital clubfoot – immunohistological analysis of the extracellular matrix."
- Laurent R.: "Interet de la kinesitherapie complementaire au sein de la methode de Ponseti dans le traitement du pied bot varus equin congenital."
Here is the list in the order you provided:
- Scarpa A. "Memoria chirurgia sui piedi torti congenita"
- Ponseti I.V.: „Congenital Clubfoot. Fundamentals of treatment.” (2nd edition
- Clubfoot model: ow
- Muscular atrophy: own
- Ippolito E., Gorgolini G.: „Clubfoot pathology in fetus and pathogenesis. A new pathogenetic theory based on pathology, imaging findings and biomechanics-a narrative review.”
- Others: own