Matthew Grol


Assistant Professor
Postdoc. Baylor College of Medicine
PH.D. University of Western Ontario
B.M.Sc. University of Western Ontario

See Publications by Matthew W. Grol on PubMed

Osteoarthritis (OA) is a degenerative joint disease characterized by loss of articular cartilage, subchondral bone sclerosis, and low-grade inflammation with synovitis. In turn, these changes lead to chronic pain and functional impairments. While often associated with age and joint injury, OA of early onset also occurs in genetic disorders of connective tissues such as chondrodysplasia. Despite the considerable socioeconomic and health impacts of OA in Canada, there are no disease-modifying therapies. Instead, mainstays of treatment are limited to pain reduction, physical therapy, and, in end stage disease, joint replacement. As such, there is significant need for therapies that prevent OA progression, provide pain relief, and reverse established disease.

 To achieve this goal, my lab focuses on several interrelated projects that employ surgical and genetic mouse models in combination with gene therapy approaches to identify targets and develop strategies to stop and reverse disease progression in OA as well as other musculoskeletal disorders.


  1. Gene therapy strategies post-traumatic and genetic forms of OA. The lab utilizes surgical approaches to model post-traumatic OA, and genetic mouse models with extracellular matrix and growth factor signaling deficits to mimic early-onset disease. In this context, we examine how gene therapy strategies can be used to modulate pathological processes to slow OA progression and block associated pain and motor impairments.
  2. Mechanisms of pain and motor impairment in OA and rare musculoskeletal diseases. Chronic pain and motor impairment are observed in a variety of musculoskeletal diseases, including osteogenesis imperfecta and OA. Work in the lab focuses on understanding how innervation and pain pathways are altered in mouse models of these diseases, and whether these pathways can be targeted therapeutically to block pain and motor deficits.
  3. Tendon and ligament development and disease. Tendons and ligaments – composed of an extracellular matrix rich in type I collagen – are critical for joint stability and function. In this regard, mice deficient in collagen chaperones such as CRTAP develop hallmarks of tendinopathy, including hypercellularity, altered collagen fibril size and organization, and reduced biomechanical strength. In this context, the lab examines how tendon and ligament pathologies contribute to joint failure and OA onset using genetic mouse models of musculoskeletal diseases.



Grol, M. W., Haelterman, N. A., Munivez, E. M., Archer, M., Hudson, D., Tufa, S. F., Keene, D. R., Eyre, D., Lee, B. H. (2020) Tendon and motor phenotypes in the Crtap-/- mouse model of recessive Osteogenesis Imperfecta. bioRxiv. doi:10.1101/2020.04.21.048488.

Stone, A.*, Grol, M. W.*, Ruan, M. Z. C., Dawson, B., Chen, Y., Jiang, M., Song, I., Jayaram, P., Cela, R., Gannon, F., Lee, B. H. (2019) Combinatorial Prg4 and Il-1ra gene therapy protects against hyperalgesia and cartilage degeneration in post-traumatic osteoarthritis. Human Gene Therapy. 30(2), 225-235.

Nixon, A. J.*, Grol, M. W.*, Lang, H. M., Ruan, M. Z. C., Stone, A., Begum, L., Chen, Y., Dawson, B., Gannon, F., Plutizki, S., Lee, B. H., Guse, K. (2018) Disease-modifying osteoarthritis treatment with interleukin-1 receptor antagonist gene therapy in small and large animal models. Arthritis and Rheumatology. 70(11), 1757-1768.

Grol, M. W., Lee, B. H. (2018) Gene therapy for repair and regeneration of bone and cartilage. Current Opinion in Pharmacology. 40, 59-66.

Grol, M. W., Stone, A., Ruan, M. Z. C., Guse, K., Lee, B. H. (2017) Chapter 8 – Prospects of gene therapy for skeletal diseases. In Thakker, R.V., Whyte, M.P., Eisman, J.A., and Igarashi, T. (Eds.), Genetics of Bone Biology and Skeletal Disease (edn 2), Academic Press, 119-137.