Histone acetylation is an important epigenetic mechanism that controls expression of certain genes. It includes non-sequence-based changes of chromosomal regional structure that can alter the expression of genes. Acetylation of histones is controlled by the activity of two groups of enzymes: the histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDACs remove acetyl groups from the histone tail, which alters its charge and thus promotes compaction of DNA in the nucleosome. HDACs render the chromatin structure into a more compact form of heterochromatin, which makes the genes inaccessible for transcription. By altering the transcriptional activity of bone-associated genes, HDACs control both osteogenesis and osteoclastogenesis. This review presents an overview of the function of HDACs in the modulation of bone formation. Special attention is paid to the use of HDAC inhibitors in mineralized tissue regeneration from cells of dental origin.
Keywords: ADSCs, adipose tissue-derived stem cells; ALP, alkaline phosphatase; BSP, bone sialoprotein; Bone regeneration; COL1, type I collagen; DMP1, dentin matrix acidic phosphoprotein 1; DPSCs, dental-derived stem cells; DSPP, dentin sialophosphoprotein; Dentin formation; Epigenetic; GSK-3, glycogen synthase kinase; HAT, histone acetyltransferase; HDAC, histone deacetylase; Histone acetyltransferase; Histone deacetylase; MSCs, mesenchymal stem cells; NaB, sodium butyrate; OCN, osteocalcin; OPN, osteopontin; PCL/PEG, polycaprolactone/polyethylene glycol; RUNX2, runt-related transcription factor 2; SOST, sclerostin; TGF-β/BMP, transforming growth factor-β/bone morphogenetic protein; TSA, Trichostatin A; VPA, valproic acid; WNT/β-catenin, Wingless-int; hPDLCs, human periodontal ligament cells.