Annals of anatomy = Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft最新文献

The International Federation of Associations of Anatomists (IFAA) and its Federative International Committee for Equality and Diversity in Anatomy (FICEDA) recommended that terms relation to pudere (to be ashamed) should be removed from Terminologia Anatomica (TA) for 3 reasons: 1) they are unscientific and outside the descriptive objectivity of science; 2) biologists should not regard as 'shameful' the essential functions undertaken by structures in the perineum; 3) the terms have sexist connotations that lie beyond the principles of Equity, Diversity and Inclusivity (EDI) in the anatomical sciences. The IFAA Executive subsequently required the Federative International Programme for Anatomical Terminology (FIPAT) to make ALL necessary changes to terms derived from pudere. However, only partial changes were enacted by FIPAT. The matter is presently unresolved and has provoked controversy. This article provides a review of the course of events and offers arguments against those criticisms levelled against changing pudere-related terms. In light of the IFAA's EDI principles, and as social thought and practice generally evolve, it is essential that the terminology on pudere is altered to reflect acceptable and unapologetic norms.

Our understanding of the molecular pathogenesis of osteoarthritis has evolved substantially over the past 20 years, but the study of osteoarthritis (OA) is much older. In the mid 19th century in-depth anatomical studies of the pathological changes in the joint were published, showing that multiple tissues were affected. These included splitting, fibrillation and loss of articular cartilage; thickening of the synovium and capsule; new bone formation (osteophytes); and subchondral bone sclerosis. Later, with the development of improved imaging, this extended to recognising changes in ligament insertions, the fat pads, and regions of oedema of the subchondral bone. Together these cause pain and loss of joint function. Many proposals have been put forward to account for why tissues change in OA. From epidemiological studies it is hard to deny that the most important factor in OA development is mechanical stress although there has been a reluctance by the research community to accept this as a unifying driver of OA joint biology. The advent of agnostic molecular profiling of OA patient tissues at scale, detailed clinical phenotyping and recognition of shared pathways across scientific disciplines has greatly accelerated discovery. Arguably a compelling new hypothesis for OA pathogenesis is emerging that aligns with the epidemiology, biomechanics, biology and genetic studies. This perspective represents a non-systematic, but evidence-based account of the role of mechanobiological pathways in OA pathogenesis, which have important implications for future treatments.

Introduction: The tendon-bone insertion represents one of nature's most elegant solutions to connecting soft and hard materials. Attaching compliant tendon tissue (elastic modulus ∼0.5 GPa) to rigid bone (elastic modulus ∼20 GPa) poses a fundamental engineering challenge due to stress concentrations at the interface. Through millions of years of evolution, the enthesis has developed sophisticated structural and compositional gradients enabling efficient load transfer while withstanding millions of loading cycles.

Main part: This perspective synthesizes recent advances in understanding the microstructural architecture, mechanical behavior, and molecular composition of the enthesis, emphasizing the Achilles tendon-calcaneus interface. Three key evolutionary strategies characterize this interface: (a) geometric refinement within a ∼500 micrometer wide zone where tendon fibers splay and subdivide from 105 micrometer to 13 micrometer thin diameter interface fibers before attaching to bone, (b) compositional gradation with collagen transitioning from type I (tendon) to predominantly type II (interface), and (c) mechanical heterogeneity with higher interface compliance contributing to energy dissipation and biomechanical robustness. Proteomic analysis identified over 400 interface proteins, with 22 significantly enriched in the enthesis. Lineage tracing revealed Gli1 + progenitor cells crucial for regeneration, while transcriptomics showed the interface resembles articular cartilage more than tendon. These insights support biomimetic material design and tissue engineering strategies.

Conclusions: Understanding nature's design principles for hard-soft interfaces provides a blueprint for next-generation biomaterials and regenerative therapies. Future advances in spatial omics, advanced imaging, and computational modeling will continue revealing secrets of this remarkable tissue, inspiring innovations in materials science, engineering, and medicine.

Background: This study aimed to developed and validated a deep-learning method for instance-level tooth segmentation in CBCT to enhance visualization and streamline detection of dental anomalies.

Methods: The proposed deep learning model was trained in segmenting teeth in scans on data from 470 scans with various dental anomalies (e.g. caries, missing teeth, bone island, periapical periodontitis) or dental histories (e.g. filling, restoration, root canal surgery). Training involved an accelerated annotation procedure in which experts annotated some of the images in the dataset, which helped the model annotate the remaining images. Experienced dentists identified anomalies and pathologies in another 60 scans after manual interpretation or segmentation by the deep learning model.

Results: The trained model required 7.025 ± 2.885sec to segment teeth in a single scan with an accuracy of 0.934 ± 0.045 on the Jaccard index and mean relative volume difference of 0.075 ± 0.066. When aided by the segmentation overlays, dentists reduced anomaly-reading time by 20%.

Conclusions: The proposed deep-learning framework achieves fully automated, instance-level segmentation of individual teeth in CBCT volumes with high geometric fidelity and clinically acceptable processing time. The high accuracy of the system supports its potential as a reliable tool in general dentistry.

This article reviews our current state of knowledge about friction, lubrication and wear of articular cartilage in diarthrodial joints, in relation to osteoarthritis. The main conclusion from this review is that the primary functional role of synovial fluid is to reduce the propensity of articular cartilage against wear from cyclical compression, not cyclical friction, though they are concurrent during normal joint motion. Contrary to widespread concepts about the role of synovial fluid, its primary function is not to reduce the friction coefficient of cartilage against cartilage, which is already very low when tested in physiological buffered saline. Instead, evidence presented from our recent studies demonstrates that synovial fluid delays the onset of delamination damage under reciprocating compressive contact, and that this mechanism depends on the concentration of synovial fluid. Therefore, it appears that some molecular constituent(s) of synovial fluid is (are) responsible for this protective effect. Identifying this (these) constituent(s), which must be able to rapidly transport (in a matter of minutes) into the top few hundreds of microns from the articular surface to impart their protective effect to the middle zone of cartilage, may become an important objective of future investigations. These findings may alter our understanding of the mechanical factors that might lead to the onset of osteoarthritis, by placing a greater emphasis on the synthesis and concentration of these molecular constituents in situ.