MechE PhD Prospectus Defense: Pooja Chainani
- Starts: 1:00 pm on Thursday, June 12, 2025
- Ends: 3:00 pm on Thursday, June 12, 2025
ABSTRACT: Tendinopathy, a painful condition resulting from repetitive damage, accounts for 30-50% of musculoskeletal injuries, affects 127 million people annually, and disrupts mobility, particularly among the athletic and aging populations. Clinical diagnosis is limited to the later stages of the condition, typically only when macro-scale damage is detectable and has reached irreversible degeneration. Despite its high prevalence, the initiating damage mechanisms that drive the progression of degeneration are poorly understood. Tendon’s function is derived from its multi-scale organization, enabling its force transmission, fatigue resistance, and viscoelastic properties. While previous literature has identified possible structural damage mechanics, the direct link between the primary initiating structural mechanisms and in vivo tendon mechanical impairment is lacking. Repetitive mechanical injuries combined with insufficient recovery leave tendons prone to injury and disrupt their innate remodeling processes. While tendinopathy is widely considered to be a degenerative condition, recent literature suggests a key role of inflammation, particularly in the earlier stages of tendinopathy. Therefore, the objective of this proposal is to investigate the primary mechanobiological and structural drivers of tendon damage in the early stages of tendon overload injuries, with a particular focus on tendon’s multi-scale hierarchy in relation to in vivo mechanics with imaging and constitutive modeling. We aim to (1) establish and validate an in vivo tendon injury animal model through physiologically relevant, noninvasive overload cyclic injuries. Through this project, we will investigate the tendon’s acute healing and load-dependent mechanobiological responses. Next, we will (2) evaluate the multi-scale structural and compositional contributions to in vivo mechanical changes during the inflammatory phase of healing. Lastly, we will (3) develop a physiologically relevant multi-scale constitutive model to predict in vivo tendon damage and repair. This work will have significant contributions to understanding initiating factors of damage biomarkers on early tendon dysfunction to potentially guide clinical strategies for early intervention and diagnosis.
COMMITTEE: ADVISOR/CHAIR Professor Ara Nazarian, ME/Orthopaedic Surgery, Harvard Medical School; Professor Brianne Connizzo, BME/ME; Professor Michael Albro, ME/MSE/BME; Professor Katherine Yanhang Zhang, ME/BME/MSE
- Location:
- ENG 245, 110 Cummington Mall
- Hosting Professor
- Nazarian