High Tibal Osteotomy (HTO)

Our research examines the possibility of slowing, stopping or reversing degenerative joint disease by altering joint biomechanics.

Abnormal joint biomechanics due to injury or anatomy predisposes to degenerative joint disease. Although previous studies reveal how biomechanics varies in normal individuals and how this changes in specific disease states, the mechanisms that cause abnormal biomechanics to induce joint degeneration are not well understood.

Understanding intervention

While many surgical and rehabilitation interventions are based on the premise that restoring joint biomechanics will protect against joint degeneration, evidence for this is lacking particularly how and when to intervene. Such evidence is particularly important to inform decisions about early and possibly traumatic surgical interventions.

Our research assesses patient specific functional and biological responses to mechanical loading in a human model of joint realignment - high tibial osteotomy (HTO) surgery.  This will correlate biological and functional indicators of altered joint biomechanics and provide evidence for protective effects of joint stabilisation/realignment.

The novelty is to relate changes in loading pre and post HTO to changes in biological (tissue, serum, urine and joint fluid) responses in a patient-specific longitudinal manner and use this to determine:

  • how altered joint biomechanics leads to knee osteoarthritis (OA)
  • the biomechanical and biological indicators of knee preserving effects after joint realignment.

Joint wear

HTO, routinely performed by three Cardiff surgeons with established reputations in this field, offers a unique opportunity to investigate the influence of joint realignment on biology, function and biomechanics in a human in vivo model. 

Knee OA predominantly affects the medial compartment and is associated with joint varus deformity (bowed legs) and biomechanical abnormalities, which can be measured using the peak external knee adduction moment (EKAM) indicating medial compartment loading and knee adduction angular impulse (KAAI) reflecting joint wear. HTO realigns the joint based on angles calculated from static X-rays, by introducing a wedge into the tibia, potentially preventing further joint degeneration by shifting the mechanical forces.

We are modelling gait cycle dynamics, EKAM and KAAI, and developing imaging, musculoskeletal models (MSMs) and finite element models (FEMs) to determine subject specific distribution of stress/strain in the subchondral bone, cartilage and meniscus of the tibia pre- and post- HTO. HTO does not involve traumatic injury within the joint capsule and is therefore ideal to measure biological effects of loading longitudinally.

We are investigating targeted and global mechanically regulated biomarkers and signals in joint fluids, blood, urine and in the subchondral bone.

Ultimately, we will relate changes in biomechanics and joint stress/strain with novel mechanically regulated biomarkers in a subject specific way.

This multidisciplinary programme has generated a new set of methodologies facilitated by a multiple protocol ethical approval. We believe there are no other groups worldwide currently have the capacity, personnel, and ethics to perform these studies.