Clinical Dilemmas in the Differential Diagnosis of Peri-implantitis: Case Presentation and Literature Review.

Advancements in the field of implantology have made dental implants a mainstay treatment for both fully and partially edentulous patients. As a result, practitioners need to be able to identify clinical signs of peri-implant disease in its early stages and provide patients with reliable treatment options. The objective of this article is to provide a differential diagnosis of peri-implant lesions, outlining the clinical, radiographic, and histopathologic features of similar benign and malignant conditions. Additionally, two case studies are presented that showcase lesions that mimic peri-implantitis, providing practitioners with practical examples of how to apply the discussed features in a clinical setting. Lesions described in the differential diagnosis include physiologic bone loss, implant fracture, loosened abutments, pyogenic granuloma, peripheral giant cell granuloma, peripheral ossifying fibroma, squamous cell carcinoma, and metastasis extending to the oral cavity.

Lineage-specific mutation of Lmx1b provides new insights into distinct regulation of suture development in different areas of the calvaria.

The calvaria (top part of the skull) is made of pieces of bone as well as multiple soft tissue joints called sutures. The latter is crucial to the growth and morphogenesis of the skull, and thus a loss of calvarial sutures can lead to severe congenital defects in humans. During embryogenesis, the calvaria develops from the cranial mesenchyme covering the brain, which contains cells originating from the neural crest and the mesoderm. While the mechanism that patterns the cranial mesenchyme into bone and sutures is not well understood, function of Lmx1b, a gene encoding a LIM-domain homeodomain transcription factor, plays a key role in this process. In the current study, we investigated a difference in the function of Lmx1b in different parts of the calvaria using neural crest-specific and mesoderm-specific Lmx1b mutants. We found that Lmx1b was obligatory for development of the interfrontal suture and the anterior fontanel along the dorsal midline of the skull, but not for the posterior fontanel over the midbrain. Also, Lmx1b mutation in the neural crest-derived mesenchyme, but not the mesoderm-derived mesenchyme, had a non-cell autonomous effect on coronal suture development. Furthermore, overexpression of Lmx1b in the neural crest lineage had different effects on the position of the coronal suture on the apical part and the basal part. Other unexpected phenotypes of Lmx1b mutants led to an additional finding that the coronal suture and the sagittal suture are of dual embryonic origin. Together, our data reveal a remarkable level of regional specificity in regulation of calvarial development.

Candidate positive targets of LHX6 and LHX8 transcription factors in the developing upper jaw.

Craniofacial development is controlled by a large number of genes, which interact with one another to form a complex gene regulatory network (GRN). Key components of GRN are signaling molecules and transcription factors. Therefore, identifying targets of core transcription factors is an important part of the overall efforts toward building a comprehensive and accurate model of GRN. LHX6 and LHX8 are transcription factors expressed in the oral mesenchyme of the first pharyngeal arch (PA1), and they are crucial regulators of palate and tooth development. Previously, we performed genome-wide transcriptional profiling and chromatin immunoprecipitation to identify target genes of LHX6 and LHX8 in PA1, and described a set of genes repressed by LHX. However, there has not been any discussion of the genes positively regulated by LHX6 and LHX8. In this paper, we revisited the above datasets to identify candidate positive targets of LHX in PA1. Focusing on those with known connections to craniofacial development, we performed RNA in situ hybridization to confirm the changes in expression in Lhx6;Lhx8 mutant. We also confirmed the binding of LHX6 to several putative enhancers near the candidate target genes. Together, we have uncovered novel connections between Lhx and other important regulators of craniofacial development, including Eya1, Barx1, Rspo2, Rspo3, and Wnt11.