Joy Chang

All Publications

• Management of a geminated tooth and supernumeraries in a patient with Acromesomelic Dysplasia, Maroteaux type. Journal of clinical orthodontics : JCO Chang, J., Azami, N., Chen, P. J., Yadav, S. 2025; 59 (8): 518-526

  View details for PubMedID 41109857

• The effect of alveolar decortication on orthodontically induced root resorption. The Angle orthodontist Chen, P. J., Chang, J. H., Dutra, E. H., Ahmida, A., Nanda, R., Yadav, S. 2020; 90 (4): 524-531

  Abstract

  To determine the effect of alveolar decortication on orthodontically induced root resorption.A total of 24 male Wistar rats (14 week old) were used. The rats were randomly divided into one of the following three groups: group 1 (control group), orthodontic tooth movement (OTM) for 2 weeks; group 2, OTM for 2 weeks + two alveolar decortications (2AD); group 3, OTM for 2 weeks + four alveolar decortications (4AD). The first molar was moved mesially for 2 weeks. Micro computed tomography was used to analyze root volume. In addition, histological sections were stained with Tartrate Resistant Acid Phosphatase (TRAP) to quantify the osteoclast number.The buccal root volume in OTM + 4AD group was decreased by 8.92% and 6.11% when compared with the OTM-only group and OTM + 2AD group, respectively. Similarly, the other four root volumes in the OTM + 4AD group was decreased by 8.99% and 5.24% when compared with the OTM-only group and OTM + 2AD group, respectively. There was a decrease in buccal root density in the OTM + 4AD group by 4.66% and 3.56% when compared with the OTM-only group and the OTM + 2AD group, respectively. In addition, there was an increase in the number of osteoclasts by 195.73% and 98.74% in OTM + 4AD group in comparison with the OTM and OTM + 2AD group.The amount of orthodontically induced root resorption was positively correlated with the extent of surgical injury used to accelerate orthodontic tooth movement.

  View details for DOI 10.2319/051819-344.1

  View details for PubMedID 33378490

  View details for PubMedCentralID PMC8028471

• Injectable RANKL sustained release formulations to accelerate orthodontic tooth movement. European journal of orthodontics Chang, J. H., Chen, P. J., Arul, M. R., Dutra, E. H., Nanda, R., Kumbar, S. G., Yadav, S. 2020; 42 (3): 317-325

  Abstract

  Accelerating orthodontic tooth movement (OTM) through biologically effective methods, such as increasing osteoclast-mediated alveolar resorption, could effectively shorten treatment time.To evaluate an injectable formulation containing receptor activator of nuclear factor kappa-B ligand (RANKL) on the OTM.We fabricated a RANKL formulation from 100 µl of 100 µg/ml RANKL adsorbed on 10 mg of poly(lactic acid-co-glycolic acid) microspheres embedded in a 10 wt% aqueous hydroxyethyl cellulose carrier gel. We characterized these formulations for the rate of RANKL release, and then tested for bioactivity using in vitro cell culture. In vivo OTM studies were conducted using 15 week old male Wistar rats for 14 days. We injected the RANKL formulations palatal to the left maxillary first molar and accomplished OTM with a nickel-titanium (NiTi) coil spring applying 5-8 g force. Control groups involved the application of NiTi coil spring with and without placebo formulation. The outcome measure included the distance of tooth movement, bone volume fraction, tissue density, and root volume determined with micro-computed tomography. We determined the amount of osteoclast activity using tartrate-resistant acid phosphatase (TRAP) staining.These formulations were able to sustain the release of RANKL for more than 30 days, and the released RANKL showed a positive effect on mice osteoclast precursor cells (RAW 264.7). Reported injectable RANKL formulations were effective in accelerating OTM compared with other control groups, with 129.2 per cent more tooth movement than no formulation and 71.8 per cent more than placebo formulation, corresponding with a significant increase in the amount of TRAP activity. We did not observe any significant differences in root resorption between the groups.Our study shows a significant increase in OTM with injectable formulations containing RANKL.

  View details for DOI 10.1093/ejo/cjz027

  View details for PubMedID 31147678

  View details for PubMedCentralID PMC7311078

• The effect of the extent of surgical insult on orthodontic tooth movement. European journal of orthodontics Chang, J., Chen, P. J., Dutra, E. H., Nanda, R., Yadav, S. 2019; 41 (6): 601-608

  Abstract

  The primary objective of this study was to investigate how the extent of surgical insult affects the orthodontic tooth movement (OTM) and the alveolar bone modelling and remodelling in a rodent model.15-week-old male Wistar rats were used in the research and they were randomly divided into three treatment groups: (1) OTM only (N = 8); (2) OTM + 2 alveolar decortication (AD) (less surgical insult) (N = 8); and (3) OTM + 4 AD (more surgical insult) (N = 8). A nickel-titanium spring delivering 5-8 g of force was used to protract the molar mesially using maxillary incisors as an anchorage. AD was done using a hand piece and a round bur, adjacent to the left first maxillary molar on the palatal alveolar bone. After 14 days of OTM Wistar rats were killed and microfocus computed tomography and histological analysis were performed.The OTM + 4AD group presented with a significant increase (P < 0.05) in the rate of tooth movement when compared to OTM + 2AD group and OTM only group. In addition, the OTM + 4AD group had a significant decrease in bone volume and tissue density (P < 0.05) and a significant increase (P < 0.05) in the trabecular spacing and trabecular thickness when compared to OTM only. Histological quantification of tartrate-resistant acid phosphatase indicated a significant percent increase (P < 0.05) in OTM + 4AD group, when compared to OTM + 2AD and OTM only group.Increased surgical insult increases the rate of OTM. Additionally, increased surgical insult decreases the bone volume and the tissue density.

  View details for DOI 10.1093/ejo/cjz006

  View details for PubMedID 30828725

  View details for PubMedCentralID PMC7317287

• "Surgery-First" Approach with Invisalign Therapy to Correct a Class II Malocclusion and Severe Mandibular Retrognathism. Journal of clinical orthodontics : JCO Chang, J., Steinbacher, D., Nanda, R., Uribe, F. 2019; 53 (7): 397-404

  View details for PubMedID 31648215

• A Genome-Wide Screen Reveals a Role for the HIR Histone Chaperone Complex in Preventing Mislocalization of Budding Yeast CENP-A. Genetics Ciftci-Yilmaz, S., Au, W. C., Mishra, P. K., Eisenstatt, J. R., Chang, J., Dawson, A. R., Zhu, I., Rahman, M., Bilke, S., Costanzo, M., Baryshnikova, A., Myers, C. L., Meltzer, P. S., Landsman, D., Baker, R. E., Boone, C., Basrai, M. A. 2018; 210 (1): 203-218

  Abstract

  Centromeric localization of the evolutionarily conserved centromere-specific histone H3 variant CENP-A (Cse4 in yeast) is essential for faithful chromosome segregation. Overexpression and mislocalization of CENP-A lead to chromosome segregation defects in yeast, flies, and human cells. Overexpression of CENP-A has been observed in human cancers; however, the molecular mechanisms preventing CENP-A mislocalization are not fully understood. Here, we used a genome-wide synthetic genetic array (SGA) to identify gene deletions that exhibit synthetic dosage lethality (SDL) when Cse4 is overexpressed. Deletion for genes encoding the replication-independent histone chaperone HIR complex (HIR1, HIR2, HIR3, HPC2) and a Cse4-specific E3 ubiquitin ligase, PSH1, showed highest SDL. We defined a role for Hir2 in proteolysis of Cse4 that prevents mislocalization of Cse4 to noncentromeric regions for genome stability. Hir2 interacts with Cse4 in vivo, and hir2∆ strains exhibit defects in Cse4 proteolysis and stabilization of chromatin-bound Cse4 Mislocalization of Cse4 to noncentromeric regions with a preferential enrichment at promoter regions was observed in hir2∆ strains. We determined that Hir2 facilitates the interaction of Cse4 with Psh1, and that defects in Psh1-mediated proteolysis contribute to increased Cse4 stability and mislocalization of Cse4 in the hir2∆ strain. In summary, our genome-wide screen provides insights into pathways that regulate proteolysis of Cse4 and defines a novel role for the HIR complex in preventing mislocalization of Cse4 by facilitating proteolysis of Cse4, thereby promoting genome stability.

  View details for DOI 10.1534/genetics.118.301305

  View details for PubMedID 30012561

  View details for PubMedCentralID PMC6116949

• Total Synthesis of a Functional Designer Eukaryotic Chromosome SCIENCE Annaluru, N., Muller, H., Mitchell, L. A., Ramalingam, S., Stracquadanio, G., Richardson, S. M., Dymond, J. S., Kuang, Z., Scheifele, L. Z., Cooper, E. M., Cai, Y., Zeller, K., Agmon, N., Han, J. S., Hadjithomas, M., Tullman, J., Caravelli, K., Cirelli, K., Guo, Z., London, V., Yeluru, A., Murugan, S., Kandavelou, K., Agier, N., Fischer, G., Yang, K., Martin, J. A., Bilgel, M., Bohutski, P., Boulier, K. M., Capaldo, B. J., Chang, J., Charoen, K., Choi, W. J., Deng, P., DiCarlo, J. E., Doong, J., Dunn, J., Feinberg, J. I., Fernandez, C., Floria, C. E., Gladowski, D., Hadidi, P., Ishizuka, I., Jabbari, J., Lau, C. Y., Lee, P. A., Li, S., Lin, D., Linder, M. E., Ling, J., Liu, J., Liu, J., London, M., Ma, H., Mao, J., McDade, J. E., McMillan, A., Moore, A. M., Oh, W. C., Ouyang, Y., Patel, R., Paul, M., Paulsen, L. C., Qiu, J., Rhee, A., Rubashkin, M. G., Soh, I. Y., Sotuyo, N. E., Srinivas, V., Suarez, A., Wong, A., Wong, R., Xie, W. R., Xu, Y., Yu, A. T., Koszul, R., Bader, J. S., Boeke, J. D., Chandrasegaran, S. 2014; 344 (6179): 55-58

  Abstract

  Rapid advances in DNA synthesis techniques have made it possible to engineer viruses, biochemical pathways and assemble bacterial genomes. Here, we report the synthesis of a functional 272,871-base pair designer eukaryotic chromosome, synIII, which is based on the 316,617-base pair native Saccharomyces cerevisiae chromosome III. Changes to synIII include TAG/TAA stop-codon replacements, deletion of subtelomeric regions, introns, transfer RNAs, transposons, and silent mating loci as well as insertion of loxPsym sites to enable genome scrambling. SynIII is functional in S. cerevisiae. Scrambling of the chromosome in a heterozygous diploid reveals a large increase in a-mater derivatives resulting from loss of the MATα allele on synIII. The complete design and synthesis of synIII establishes S. cerevisiae as the basis for designer eukaryotic genome biology.

  View details for DOI 10.1126/science.1249252

  View details for Web of Science ID 000333746100050

  View details for PubMedID 24674868

  View details for PubMedCentralID PMC4033833

• Expression of EMMPRIN modulates mediators of tumor invasion in oral squamous cell carcinoma. Journal of the California Dental Association Siu, A., Chang, J., Lee, C., Lee, S., Lee, C., Ramos, D. M. 2013; 41 (11): 831-8

  Abstract

  Squamous cell carcinoma (SCC) accounts for 96 percent of all intraoral malignancies. The five-year survival rate is 50 percent and has not improved in 60 years. During SCC progression, subsets of SCC cells undergo an epithelial-to-mesenchymal transition (EMT) to become highly invasive. The extracellular matrix metalloproteinase inducer (EMMPRIN) contributes to EMT by activating local matrix metalloproteinases (MMPs). In this study, we found that EMMPRIN modulates the invasive phenotype and may be a potential therapeutic target.

  View details for PubMedID 24341135

• Alphavbeta3 suppresses the RhoA-LIMK1 pathway in K1735 melanoma. Journal of the California Dental Association Lee, C., Siu, A., Chang, J., Dang, D., Ramos, D. M. 2012; 40 (12): 921-7

  Abstract

  Mucocutaneous melanoma has a five-year survival rate of less than 10 percent. The alphavbeta3 integrin promotes invasion, which requires actin reorganization by cofilin. The authors previously showed that cofilin and alphavbeta3 promote invasion. K1735 melanoma has several clones, each with different levels of alphavbeta3. The authors found that expression of alphavbeta3 suppresses activation of RhoA thus inhibiting LIMK1 phosphorylation of cofilin. This indicates that alphavbeta3 integrin suppresses the RhoA/ ROCK/LIMK1 pathway.

  View details for PubMedID 23362664