Year: 2026
Type: article
Abstract: other malalignments of the ankle and hindfoot.Intrinsic factors, in turn, weaken ligaments and tendons, reducing their ability to withstand stress even under near-normal functional conditions.Notable intrinsic factors include specific or seronegative arthritis, inflammatory diseases, and genetic abnormalities affecting the quality of collagen matrix production.It should be emphasized that all these etiological agents act on the full spectrum of tissues responsible for stabilizing and enabling the functional performance of the various segments of the foot, without showing a preferential site for their deleterious action.[11][12][13] Pathophysiology of Progressive Collapsing Foot Deformity-Three-dimensional Anatomy and Gait Biomechanics PerspectivePCFD is not a single-structure disease but a multiplanar collapse emerging from coupled failure of dynamic (posterior tibial tendon-PTT) and static (spring/deltoid ligaments, plantar fascia) stabilizers acting on a triplanar hindfoot-midtarsal-forefoot complex.Consensus work formalized PCFD as a 3D deformity with variable mixes of hindfoot valgus, forefoot/midfoot abduction, forefoot varus, peritalar subluxation, and in advanced cases, ankle valgus-urging imaging and staging frameworks that capture multiplanar alignment under load.4,14,15 The subtalar joint (STJ) is the mechanical hinge coupling tibial rotation to hindfoot pronation-supination and managing the IntroductIonThe term "progressive collapsing foot deformity" (PCFD)conceived from an expert consensus in 2019-refers to a complex of deformities involving all anatomical regions of the foot and ankle, presenting in a heterogeneous and nonsequential pattern but with a clearly progressive nature.Its pathophysiology encompasses numerous anatomical structures-both static and dynamic-whose functional interdependence ultimately produces deformities of varying characteristics and complexity, without a linear progression pattern.1,2 Advances in our understanding of the physiology of the foot and ankle, as well as the biomechanics of gait, have rendered obsolete the decades-old concept prevailing in the literature that "adult-acquired flatfoot" could be caused solely by failure or rupture of the posterior tibial tendon (PTT).Given the PTT's critical role in maintaining the plantar vault (concept that expands the notion of the "medial longitudinal arch") and in managing the foot's transition from a flexible, adaptive structure to a rigid lever during gait, it initially seemed reasonable to identify PTT dysfunction as the principal driver in the genesis of this complex of deformities.However, observations in large patient cohorts made it evident that a significant proportion of "adult-acquired flatfoot" cases could not be attributed to PTT insufficiency, thereby enabling the identification of other primary anatomical structures responsible for the deformities.[3][4][5][6][7] It is now understood that PCFD results from the physical and functional deterioration of various stabilizing elements-key players in normal foot function-leading to a cascade in which other stabilizers are recruited to compensate (Fig. 1).These compensatory structures, subjected to progressive overload, ultimately fail in sequence, producing varied patterns and compositions of deformities.[8][9][10] The etiological factors capable of producing structural or functional defects in the elements involved in PCFD can be broadly categorized as extrinsic or intrinsic.Extrinsic factors primarily increase the forces acting on ligaments, tendons, joint capsules, cartilage, and bones through alterations in the balance and function of the foot and ankle.Examples include obesity, trauma, primary osseous deformities, idiopathic flatfoot, and
Authors: Daniel Baumfeld, Caio Nery
Language: English
Topic: Foot and Ankle Surgery
Subfield: Orthopedics and Sports Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W7150774448