Hardik Makkar, an NIH/NIDCR R90 Postdoctoral Fellow at the University of Pennsylvania School of Dental Medicine, and co-principal investigator Christopher M. Madl, Assistant Professor in Penn Engineering’s Department of Materials Science and Engineering, have been named winners of the 2026 #CiPD IDEA Prize, co-sponsored by Penn Health-Tech.
The award was announced during this year’s 2026 Center for Innovation & Precision Dentistry (#CiPD) Symposium, where Makkar presented his recent work on the nuclear mechano-regulation of gingival fibroblast transcriptional states. The symposium brought together colleagues and trainees from Penn Dental Medicine and Penn Engineering, highlighting the growing momentum behind research at the intersection of engineering, dental medicine, and precision oral healthcare.
Makkar and Madl received the prize for their project, “Gingival Filler for Precision Restorative Periodontics,” a translational biomaterials strategy designed to treat severe periodontitis by restoring the mechanical integrity of diseased gingival tissue.
Severe periodontitis affects more than one billion people worldwide and is marked by progressive destruction of the extracellular matrix, or ECM, within gingival connective tissue. This degradation is driven by host and microbial proteases and leads to tissue softening, loss of structural integrity, and sustained inflammation.
Current clinical appro aches, including mechanical debridement (commonly referred to as deep cleaning or dental scaling) and periodontal flap surgery, lower disease-causing microbial burden. While essential, these treatments do not directly repair the mechanically compromised tissue environment that can continue to fuel inflammation and limit durable healing.
Makkar and Madl’s work proposes a new direction: treating biomechanical failure as a core feature of periodontal disease.
Their project focuses on the development of a gingival ECM filler that can restore healthy tissue mechanics and homeostasis. The goal is to create a chair-side, minimally invasive intervention that complements existing periodontal care while addressing a major gap in current treatment: the damaged mechanical microenvironment.
Preliminary data from Makkar’s research show that ECM stiffness plays a key role in regulating gingival cell behavior. Gingival fibroblasts encapsulated in stiffer, healthy tissue-mimicking matrices downregulate inflammatory cytokines and adopt a more homeostatic, matrix-maintaining phenotype. These findings suggest that restoring tissue stiffness may help break the cycle of chronic inflammation and matrix destruction that defines periodontitis.
The project draws directly on the combined expertise of the two investigators. Makkar brings research experience in mechanobiology and bioengineered microphysiological systems to study periodontal host-microbe interactions. Madl’s laboratory contributes deep expertise in protein-engineered biomaterials, bioorthogonal chemistries, and hydrogel systems that enable precise control over matrix mechanics and cell–ECM interactions.
The project’s broader impact lies in its shift from reactive microbial control to proactive biomechanical maintenance. By treating ECM stiffness as an actionable therapeutic target, Makkar and Madl are advancing a new framework for chronic oral inflammatory disease: one in which biomaterials are used not simply to fill or repair tissue, but to restore the physical cues that help tissues remain healthy.