“Chronic limb disuse during the active growth phase can induce complex secondary deformities, including paradoxical bone overgrowth. A 12-month-old neutered male Toy Poodle presented with non-weight-bearing right forelimb lameness resulting from a chronic shoulder malunion following failed stabilization of a medial luxation. Computed tomography revealed a complete nonunion of the shoulder joint with severe varus deformity, alongside a significant secondary ulnar overgrowth (6.08% elongation compared with the contralateral ulna) that created a functional ‘short-radius’ configuration and elbow incongruity. A combined surgical approach was employed: shoulder arthrodesis was performed utilizing patient-specific 3D-printed osteotomy and reduction guides to ensure precise alignment and fixation at a target angle of 105°, concurrent with a proximal ulnar osteotomy to restore ulnar congruity. Postoperative recovery was rapid, with functional weight-bearing observed at 1 month. At 9 months postoperatively, the dog exhibited normal limb function without lameness, and radiographs confirmed solid arthrodesis and corrected elbow alignment. These findings remained unchanged at 15 months postoperatively. This case highlights chronic disuse as a potential etiology for paradoxical ulnar overgrowth and demonstrates a successful combined surgical strategy for the management of complex, multi-joint limb deformities.”
The authors speculate “This report is subject to the inherent limitations of a single case study. The conclusions drawn, particularly regarding the proposed mechanism of disuse-induced ulnar overgrowth, cannot be generalized to the wider population. The hypothesis that reduced physeal compression (Hueter-Volkmann principle) in the non-load-bearing ulna accelerated its growth, while the radius was primarily affected by atrophic forces (Wolff’s Law), is a compelling interpretation of the clinical data but does not establish a definitive causal relationship. A significant limitation is the lack of histopathological examination. Histology of the distal ulnar physis could have provided direct evidence of its activity, and analysis of the bone tissue could have further characterized the nature of the disuse osteopenia beyond the cross-sectional area measurements.”
However I think the growth may due to altered fluid flow.
Here’s AI speculation:
“The Normal Process: When a dog walks normally, the mechanical squeezing of the bone pushes interstitial fluid through these tiny channels. Osteocytes act as “flow sensors.” Normal, dynamic fluid shear stress signals the bone to maintain a healthy balance of remodeling—not growing too fast or too slow.
The Disuse Effect: When the dog stopped bearing weight on the limb, this dynamic, cyclical pumping mechanism vanished. The sudden absence of normal fluid shear stress can dramatically alter local signaling. In growing bones, the lack of mechanical feedback can “confuse” the growth plates (physes), disrupting the normal chemical brakes that tell the bone when to slow down its elongation.
2. Regional Vascular Stasis (The “Congestion” Theory)
A primary driver of bone overgrowth in disused limbs is actually hyperemia (increased or stagnant blood volume in the region).
In a healthy, active limb, muscle contractions act as a secondary pump to push venous blood back up toward the heart. When a limb experiences chronic disuse:
Loss of the Muscle Pump: Blood begins to pool or flow much more slowly through the metaphyseal and physeal blood vessels (the vascular networks supplying the growth plates).
Vascular Congestion: This localized “sluggish” blood flow or chronic venous congestion creates a highly specific microenvironment. It alters local oxygen tension, increases the accumulation of local growth factors, and elevates hydrostatic pressure inside the bone marrow.
Stimulating the Growth Plate: In pediatric and growing patients, this localized vascular congestion and increased resting pressure can hyper-stimulate the chondrocytes (cartilage cells) in the growth plate, causing them to divide and expand faster than they normally would, leading to paradoxical elongation.
The authors of the paper framed the overgrowth mathematically and mechanically (less compression = more growth). However, your hypothesis highlights the biological why: the loss of normal weight-bearing fundamentally alters both the micro-fluid flow past bone cells and the macro-blood flow through the limb’s vasculature. This fluid stagnation and congestion create a perfect storm of local growth factor pooling that likely supercharged the ulna’s growth plate”
This is possible evidence for the use of blood flow restriction and altering fluid flow for the basis of inducing longitudinal bone growth. I emailed the author of the paper to ask what they thought of this theory.