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Faculty Research Labs

Allen Lab

The major focus of Matthew R. Allen’s research laboratory is to understand the tissue-level mechanisms responsible for bone integrity in health and disease. We use numerous in vivo model systems to study how disease and pharmaceutical intervention influence bone structure, cellular activity, tissue-level properties (such as mineralization, microdamage, collagen, hydration), and biomechanical properties.

The laboratory studies a range of diseases/conditions, including osteoporosis, chronic kidney disease, and disuse using techniques that include imaging (CT, DXA, X-ray), histology (static and dynamic histomorphometry, microdamage), and mechanical testing (bending, compression, fatigue loading).

The laboratory work closely with faculty in biomedical engineering (Joseph Wallace) and nephrology (Sharon Moe), forming an interdisciplinary and translational research team.

The laboratory values wellness, individuality, professional development, and mentoring.

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Current Research Areas

Treatment of skeletal complications associated with chronic kidney disease (CKD)

The musculoskeletal complications of CKD have long been appreciated. Individuals with CKD are at significantly higher risk of fracture and, more strikingly, are more likely to die following fracture than are non-CKD patients.  This is due in part to the dramatic cortical bone loss that occurs. Although numerous agents exist for treating bone loss, these have not been approved for use in CKD in part because little preclinical work has been undertaken to study the safety and efficacy in the setting of compromised kidney function.  Our work has begun to close this gap in knowledge by studying the skeletal effects of treatment using a naturally occurring animal model of CKD. This work has been funded by 2 NIH R01’s, 2 VA Merit Grants, 1 industry sponsored award, and five NIH fellowships for PhD students, MD/PhD students and Post-doctoral Fellows.


Pharmaceutical effects on bone quantity and quality

A central focus of the laboratory is to understand how pharmaceutical treatments affect bone structure and function. Using various experimental models, we have contributed to a greater understanding of bisphosphonates, raloxifene, parathyroid hormone and combination therapy on properties such as remodeling, architecture, microdamage, hydration, collagen. This work has been funded by multiple NIH R01s and several industry grants.

Research funding supporting primary projects

R01-DK132101 (MPI: Nickolas, Allen, Moe)
09/01/2023 to 08/31/2027
Precision medicine approaches to renal osteodystrophy 
The goal of this project is to develop a microRNA-based approach to diagnosing and tracking changes in bone due to chronic kidney disease

VA Merit Award BX003025 (PI: Allen)
01/01/2021-12/31/2026
Treating Bone Deterioration Associated with Chronic Kidney Disease
The goal of this project is to evaluate therapies for skeletal complications associated with chronic kidney disease.

NSF 1952993 (Multi PIs: Siegmund/Allen/Wallace)
06/01/2020-05/31/2024
LEAP-HI: Engineering New Solutions to Reduce the Burden of Skeletal Fracture
The goals of this project are to determine tissue-level mechanical effects of bone hydration and to determine its potential to modify bone fracture properties.

Recent Publications

Surowiec RK, Swallow EA, Warden SJ, Allen MR. Tracking changes of individual cortical pores over 1 year via HR-pQCT in a small cohort of 60-year-old females. Bone Rep. 2022 Nov 2;17:101633. doi: 10.1016/j.bonr.2022.101633. PMID: 36337684; PMCID: PMC9634666.

Surowiec RK, Allen MR, Wallace JM. Bone hydration: How we can evaluate it, what can it tell us, and is it an effective therapeutic target? Bone Rep. 2021 Dec 21;16:101161. doi: 10.1016/j.bonr.2021.101161. PMID: 35005101; PMCID:PMC8718737.

Swallow EA, Metzger CE, Newman CL, Chen NX, Moe SM, Allen MR. Cortical porosity development and progression is mitigated after etelcalcetide treatment in an animal model of chronic kidney disease. Bone. 2022 Apr;157:116340. doi:10.1016/j.bone.2022.116340. Epub 2022 Jan 24. PMID: 35085840.

Tippen SP, Metzger CE, Swallow EA, Sacks SA, Wallace JM, Allen MR. The combination of aging and chronic kidney disease leads to an exacerbated cortical porosity phenotype. Bone. 2022 Jan;154:116228. doi: 10.1016/j.bone.2021.116228. Epub 2021 Oct 5. PMID: 34624561; PMCID: PMC8671241.

Metzger CE, Swallow EA, Stacy AJ, Tippen SP, Hammond MA, Chen NX, Moe SM, Allen MR. Reversing cortical porosity: Cortical pore infilling in preclinical models of chronic kidney disease. Bone. 2021 Feb;143:115632. doi: 10.1016/j.bone.2020.115632. Epub 2020 Sep 11. PMID: 32927105; PMCID: PMC7770083.

View a full list of publications

Research Team

5035-Allen, Matthew

Matthew R. Allen, PhD

Professor of Anatomy, Cell Biology & Physiology

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Sam Tippen

PhD Graduate Student

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Corinne E. Metzger, PhD

Assistant Research Professor of Anatomy, Cell Biology & Physiology