Az osteoporosis antirezorptív kezelésének biológiai alapjai és az állcsontok antirezorptív kezelés okozta osteonecrosisa
Absztrakt
Az ötven év feletti lakosság egyik leggyakoribb, az életminőséget súlyosan rontó állapota az osteoporosis, aminek pontos
pathomechanizmusa még a mai napig sem teljesen feltárt. Ma az életkorral együtt járó csonttömegvesztés lassításában
az egyik legelfogadott gyógyszeres terápia a csontátépülésben fontos szerepet játszó osteoclastok blokkolása, az ún.
antirezorptív szerek alkalmazása. Ezeket a szereket az osteoporosis mellett széles körben alkalmazzák metasztatikus
csonttumorok, hiperkalcémiával társuló daganatok és más, fokozott osteoclast aktivitással társuló kórképek gyógykezelésében
is. Az antirezorptív-kezelésben a leggyakrabban alkalmazott szer a biszfoszfonát csoport, azonban az utóbbi
évtizedben a szelektív RANKL (receptor activator for nuclear factor-kappa B ligand), ellenes rekombináns monoclonalis
antitest (denosumab) is széles körben alkalmazott. A két vegyület hatásmechanizmusa merőben eltérő. A biszfoszfonátok
irreverzibilisen beépülnek a csont szervetlen vázába, és a csontátépülés során az osteoclastok ezeket bekebelezik,
metabolizálják, de nem képesek teljesen lebontani. Végül olyan toxikus metabolitok képződnek a sejtben, amelyek
súlyosan károsítják a sejtek cytosceletonját, a sejt nem képes a csontmátrixra tapadni, és végül apoptosis áldozata
lesz. Ugyanakkor a denosumab a RANKL blokkolása révén az osteoclast neogenezist gátolja, és ezáltal a funkcióképes,
differenciálódott, érett osteoclastok száma csökken, Tehát, amíg a biszfoszfonátok az érett OC sejteken hatnak,
a denosumab az OC neogenezist állítja le. Az eltérő hatásmechanizmusok ellenére mindkét szer egyik, bár nem gyakori
mellékhatása az invazív fogászati kezeléseket követő csontnecrosis, angol terminológiában osteonecrosis of jaws.
Mivel mindkét szer az osteoclast aktivitást blokkolja, ezért nagy valószínűséggel a csontnecrozisért is elsősorban az OCL
sejtek aktivitásának hiánya felelős. Ma még az ONJ evidenciákon alapuló kezelése nem adott. Több alternatív kezelési
stratégiáról jelentek meg közlemények. Ezek közül az egyik a rekombináns h-PTH 1–34 hormonkészítmények (teriparatid)
alkalmazása, amely ismételten beindíthatja a korábban blokkolt összehangolt csontátépülést.
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