Impact of Myeloid p38α/MAPK on Orthodontic Tooth Movement.
Christian KirschneckHendrik NusserJonathan JantschPeter ProffAgnes SchröderPublished in: Journal of clinical medicine (2022)
Objectives : Myeloid p38α/MAPK regulate and coordinate osteoclastogenesis. The present study was conducted to investigate the role of myeloid p38α/MAPK during orthodontic tooth movement. Methods : Orthodontic tooth movement was performed in wildtype and p38α Δmyel mice lacking p38α/MAPK expression in myeloid cells. First, bone parameter as well as osteoblast and osteoclast number were determined in tibiae. RNA was isolated from the untreated and orthodontically treated maxillary jaw side and expression of genes involved in inflammation and bone remodelling were analysed. Finally, periodontal bone loss, alveolar bone density and extent of orthodontic tooth movement were assessed. Results : Bone density was increased in p38α Δmyel mice compared to wildtype mice in tibiae ( p = 0.043) and alveolar bone ( p = 0.003). This was accompanied by a reduced osteoclast number in tibiae ( p = 0.005) and TRAP5b in serum ( p = 0.015). Accordingly, expression of osteoclast-specific genes was reduced in p38α Δmyel mice. Extent of tooth movement was reduced in p38α Δmyel mice ( p = 0.024). This may be due to the higher bone density of the p38αΔmyel mice. Conclusions : Myeloid p38α/MAPK thus appears to play a regulatory role during orthodontic tooth movement by regulating osteoclastogenesis.
Keyphrases
- bone loss
- high fat diet induced
- bone mineral density
- dendritic cells
- poor prognosis
- bone marrow
- acute myeloid leukemia
- soft tissue
- gene expression
- insulin resistance
- induced apoptosis
- postmenopausal women
- dna methylation
- transcription factor
- inflammatory response
- metabolic syndrome
- immune response
- cell death
- signaling pathway
- endoplasmic reticulum stress
- genome wide identification