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B-type glenoids are characterized by posterior humeral head migration and/or bony-erosion-induced glenoid retroversion. Patients with this type of osteoarthritic glenoids are known to be at increased risk of glenoid component loosening after anatomic total shoulder arthroplasty (aTSA). One of the main challenges in B glenoid surgical planning is to find a balance between correcting the bony shape and maintaining the quality of the bone support. This study aims to systematically quantify variabilities in terms of scapular morphology and bone mineral density in patients with B glenoids and to identify patterns of covariation between these two features. Using computed tomography scan images of 62 patients, three-dimensional scapular surface models were constructed. Rigid and nonrigid surface registration of the scapular surfaces, followed by volumetric registration and material mapping, enabled us to develop statistical shape model (SSM) and statistical density model (SDM). Partial least square correlation (PLSC) was used to identify patterns of covariation. The developed SSM and SDM represented 85.9% and 56.6% of variabilities in terms of scapular morphology and bone density, respectively. PLSC identified four modes of covariation, explaining 66.0% of the correlation between these two variations. Covariation of posterior-inferior glenoid erosion with posterior sclerotic bone formation in association with reduction of bone density in the anterior and central part of the glenoid was detected as the primary mode of covariation. Identification of these asymmetrical distribution of bone density can inform us about possible reasons behind glenoid component loosening in B glenoids and surgical guidelines in terms of the compromise between bony shape correction and bone support quality., SCOPUS: ar.j, info:eu-repo/semantics/published

Background: An important reason for failure of anatomic total shoulder arthroplasty is glenoid component loosening. We investigated the effect of backside bone support on the risk of failure of a glenoid component. Methods: A finite element model was developed. Virtual surgery was performed for 2 types of glenoid components (cemented all polyethylene [PE] vs. metal backed [MB]), both with gradually decreasing backside bone support. Both bone failure and fixation failure were analyzed. The percentages of bone failure and fixation failure in terms of the critical cement volume (CCV) and micromotion-threshold percentage ratio (MTPR) for the PE and MB components, respectively, were defined and compared. Results: For the reference PE model, the percentages of bone failure and fixation failure (CCV) were 17% and 34%, respectively. With eccentric loading for the MB component, the percentages of bone failure and fixation failure (MTPR) were 6% and 3%, respectively. A global increase in failure was observed with decreasing bone support. The increase in fixation failure, starting from the reference values (MTPR vs. CCV), was relatively more pronounced for the MB component (136% vs. 128%). Discussion: Decreasing backside bone support for an anatomic glenoid component leads to an increased risk of fixation and bone failure. For PE components, decreasing backside support to 95% bone support had only a limited effect. In the case of an MB component, we noticed an increase in micromotion and bone failure already starting from 97% bone support. We conclude that an anatomic glenoid component should always be implanted while maximizing backside bone support., SCOPUS: ar.j, info:eu-repo/semantics/published

To further explore the allelic heterogeneity within the group of LEMD3-related disorders, we have screened a larger series of patients including 5 probands with osteopoikilosis or Buschke-Ollendorff syndrome (BOS), 2 families with the co-occurrence of melorheostosis and BOS, and 12 unrelated patients with isolated melorheostosis. Seven novel LEMD3 mutations were identified, all predicted to result in loss-of-function of the protein. We confirm that loss-of-function mutations in the LEMD3 gene can result in either osteopoikilosis or BOS. However, LEMD3 germline mutations were only found in two melorheostosis patients belonging to a different BOS family and one sporadic patient with melorheostosis. The additional presence of osteopoikilosis lesions in these patients seemed to distinguish them from the group of sporadic melorheostosis patients where no germline LEMD3 mutation was identified. Somatic mosaicism for a LEMD3 mutation in the latter group was also not observed, and therefore we must conclude that the genetic defect in the majority of sporadic and isolated melorheostosis remains unknown.

To further explore the allelic heterogeneity within the group of LEMD3-related disorders, we have screened a larger series of patients including 5 probands with osteopoikilosis or Buschke-Ollendorff syndrome (BOS), 2 families with the co-occurrence of melorheostosis and BOS, and 12 unrelated patients with isolated melorheostosis. Seven novel LEMD3 mutations were identified, all predicted to result in loss-of-function of the protein. We confirm that loss-of-function mutations in the LEMD3 gene can result in either osteopoikilosis or BOS. However, LEMD3 germline mutations were only found in two melorheostosis patients belonging to a different BOS family and one sporadic patient with melorheostosis. The additional presence of osteopoikilosis lesions in these patients seemed to distinguish them from the group of sporadic melorheostosis patients where no germline LEMD3 mutation was identified. Somatic mosaicism for a LEMD3 mutation in the latter group was also not observed, and therefore we must conclude that the genetic defect in the majority of sporadic and isolated melorheostosis remains unknown.

To further explore the allelic heterogeneity within the group of LEMD3-related disorders, we have screened a larger series of patients including 5 probands with osteopoikilosis or Buschke-Ollendorff syndrome (BOS), 2 families with the co-occurrence of melorheostosis and BOS, and 12 unrelated patients with isolated melorheostosis. Seven novel LEMD3 mutations were identified, all predicted to result in loss-of-function of the protein. We confirm that loss-of-function mutations in the LEMD3 gene can result in either osteopoikilosis or BOS. However, LEMD3 germline mutations were only found in two melorheostosis patients belonging to a different BOS family and one sporadic patient with melorheostosis. The additional presence of osteopoikilosis lesions in these patients seemed to distinguish them from the group of sporadic melorheostosis patients where no germline LEMD3 mutation was identified. Somatic mosaicism for a LEMD3 mutation in the latter group was also not observed, and therefore we must conclude that the genetic defect in the majority of sporadic and isolated melorheostosis remains unknown.