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Genetic Predisposition to External Apical Root Resorption in Orthodontic Patients: Linkage of Chromosome-18 Marker

¹ Department of Oral Facial Development, Indiana University School of Dentistry, 1121 West Michigan Street, Indianapolis, IN 46202-5186, USA;
² Department of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, USA;

View larger version (56K): [in this window] [in a new window]   Figure 1. Transmission of D18S64 alleles in three families, each with two offspring who underwent orthodontic treatment. (Panel A) Pedigree. Circles denote females, squares denote males, and the 1, 2, 3, and 7 alleles within indicate the D18S64 genotype. Roman numeral (I) denotes parents and (II) denotes offspring. Arabic numbers below indicate the individual number. External apical root resorption (EARR) values, in millimeters, for the maxillary central incisors in treated offspring are shown. (Panel B) Polyacrylamide gel electrophoresis of PCR products derived from all individuals in the pedigrees. Each lane corresponds to the individual in the pedigree shown above in panel A. Band sizes in basepairs (bp) are indicated on the left (188 bp = allele 1, 190 bp = allele 2, 192pb = allele 3, and 206 bp = allele 7). (Panel C) Pre-treatment (Pre) and post-treatment (Post) lateral cephalograms for treated siblings (AII-3 and AII-4) in Family A. Apices of the roots of the central incisors and the incisal edges are indicated with upper and lower arrows, respectively.

View larger version (17K): [in this window] [in a new window]   Figure 2. Two proposed pathways for osteoclast formation in relation to EARR associated with orthodontic treatment. One pathway is RANK-dependent, while the other one might be mediated by TNFR1 and/or TNFR2 (tumor necrosis factor receptor). RANK is the intrinsic cell-surface determinant that mediates the effects of RANK ligand (RANKL) and osteoprotegerin (OPG) on bone resorption as well as the effects of cytokines like IL-1β. RANKL (also known as ODF and OPGL), expressed on the surfaces of pre-osteoblastic cells, binds to RANK on the osteoclastic precursor cells and is critical for differentiation, fusion, activation, and survival of osteoclastic cells. OPG (also known as OCIF) puts a brake on the entire system by blocking the effects of RANKL. The pro-resorptive cytokine lL-1β modulates this system by directly increasing the RANKL expression. Two main components of this pathway (IL-1β and a marker closely linked to RANK) were found to be in linkage disequilibrium and/or genetically linked to EARR associated with orthodontic treatment. This suggests that osteoclasts stimulated through this pathway are related to root resorption during orthodontic tooth movement. In contrast, TNF in the second pathway is able to induce osteoclast formation in the RANK-independent pathway, presumably by activation of either TNFR1 and/or TNFR2. The absence of association of TNF with EARR in the current study and in previous studies suggests that osteoclastic cells induced through this pathway are not related to root resorption during orthodontic treatment.

Journal of Dental Research, Vol. 82, No. 5, 356-360 (2003)
DOI: 10.1177/154405910308200506


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