Growth factors, genes, bone proteins and apoptosis in the temporomandibular joint (TMJ) of children with ankylosis and during disease recurrence.

UNLABELLED: AIM OF STUDY was complex detection of appearance and distribution of growth factors, facial bone growth stimulating genes, ground substance proteins and apoptosis in bone of ankylotic TMJ in primary and repeatedly operated children.

MATERIALS AND

METHODS

Ankylotic tissue was obtained during the arthroplastic surgery from two 6 years old children (boy and girl) with osseous type of disease. The girl underwent the repeated surgery in TMJ due to the same diagnosis in age of 12 years. Ankylotic tissue was proceeded for detection of BMP2/4, TGFβ, Msx2, osteopontin, osteocalcin immunohistochemically, and apoptosis. RESULTS demonstrated massive bone formation intermixed by neochondrogenesis the lack of BMP 2/4, but abundant number of TGFβ-containing cells in bone of all tested cases. Despite rich osteopontin positive structures in bone obtained from both - primary and repeated surgery, osteocalcin demonstrated variable appearance in 6 years aged children, but was abundant in joint 5 years later during disease recurrence. Expression of Msx2 varied widely before, but with tendency to decrease stabilized until few positive cells in bone of 12 years old girl. Apoptosis practically was not detected in primarily operated TMJ, but massively affected the supportive tissue in girl with recurrent ankylosis.

CONCLUSIONS

The lack of BMP2/4 expression in ankylotic bone proves the disorders in cellular differentiation with simultaneous compensatory intensification of cellular proliferation and/or growth by rich expression of TGFβ leading to the remodelling of TMJ. Mainly rich distribution of osteocalcin and osteopontin indicate the intensive mineralization processes of ankylotic bone. Persistent Msx2 expression is characteristic for the supportive tissue of recurrent ankylosis of TMJ and indicates the persistent stimulation of bone growth compensatory limitated by massive increase of programmed cell death.