Mkx, also known as Mohawk homeobox, is a transcription factor. It is crucial for tendon fibril growth post-natally and plays a significant role in maintaining the homeostasis of various tissues, including the periodontal ligament (PDL) [4,5]. It is involved in pathways related to tenogenic differentiation, bone remodeling, and may have associations with drug response in colorectal cancer [2,3]. Genetic models, such as knockout mice, are valuable tools for studying Mkx's functions.

In Mkx-deficient rats, orthodontic tooth movement was significantly reduced, with fewer osteoclasts on the compression side, suggesting Mkx's role in osteoclast induction during orthodontic tooth movement [1]. Mkx-deficient mice exhibited ectopic ossification in the Achilles tendon, resulting from aberrant differentiation of tendon progenitor cells, highlighting its role in tendon tissue homeostasis [4]. In the PDL, single-cell RNA sequencing of Mkx knockout rats showed up-regulation of ossification-related genes in mesenchymal and osteoblast clusters, and increased inflammatory mediators in macrophage clusters, indicating its importance in PDL homeostasis [5].

In conclusion, Mkx is essential for maintaining tissue homeostasis, especially in tendons and the PDL. Gene knockout mouse models have revealed its role in orthodontic tooth movement, tendon ossification, and PDL function, which could potentially contribute to understanding and treating related diseases such as periodontitis and tendon ossification [1,4,5,6].