ABSTRACT
Methods@#For simulating BRONJ, zoledronic acid was administered to 40 rats for 5 weeks. Two weeks later, a right first molar was extracted from each rat. The rats were randomized into four groups of socket treatments: control (empty extraction socket) or with sockets filled with ACS, HA, or HA+ACS (n=4×10). After 2 weeks, 5 rats in each group were sacrificed and subjected to histopathologic and histomorphometric evaluation. Eight weeks post-surgically, the rest of rats were euthanized and histologically examined. The Kruskal-Wallis test was used to compare the four treatments at each time point (α=0.05). @*Results@#Six rats were lost overall. In the second week, vascularization was higher in ACS group (P0.05); empty lacunae were the most and fewest in control and HA+ACS groups, respectively (P0.05). In the eighth week, vascularization was not different in groups (P>0.05); the highest and lowest osteoclast activities were seen in the control and HA+ACS groups, respectively (P<0.05); empty lacunae were the most and fewest in control and HA+ACS, respectively (P<0.05); maximum and minimum numbers of eosinophils were in control and HA+ACS groups, respectively (P<0.05); HA and control groups exhibited the highest and lowest lymphocyte counts, respectively (P<0.05); the lowest and highest neutrophil counts were observed in HA+ACs and control groups, respectively (P<0.05); and the highest and lowest extents of the live bone were observed in HA+ACS and control groups, respectively (P<0.05). @*Conclusions@#Within the limitations of this preliminary animal study, HA and especially HA+ACS seem a proper method for preventing or treating BRONJ.
ABSTRACT
Infantile malignant osteopetrosis [arOP] is an autosomal recessive disorder. Mutations in the T-cell immune regulator 1 [TCIRG1] gene were found as the cause of arOP. We found the first Iranian patient with a rare gross deletion in this gene. The patient was a 5-year-old girl with macrocephaly, facial dysmorphism, blindness, mental retardation, hepatosplenomegaly, pancytopenia, and osteosclerotic changes in the skull and limb. Molecular analysis was performed using reverse transcriptase-polymerase chain reaction for exons 10-19 of the TCIRG1 gene followed by whole gene sequencing. She showed a 275 bp unexpected amplified segment. Sequencing revealed a gross deletion in exons 10-15 transcript region of TCIRG1 that affected codon 389 to 518. Various types of mutations in the TCIRG1 gene in arOP have been reported, however, gross deletions are reported rarely. This gross deletion is the first mutation reported among Iranian patients in this gene. This deletion is also the largest deletion of TCIRG1 gene reported to date