| Literature DB >> 33275027 |
Pablo A Slullitel1, Daniel Coutu2, Martin A Buttaro1, Paul Edgar Beaule3, George Grammatopoulos3.
Abstract
As our understanding of hip function and disease improves, it is evident that the acetabular fossa has received little attention, despite it comprising over half of the acetabulum's surface area and showing the first signs of degeneration. The fossa's function is expected to be more than augmenting static stability with the ligamentum teres and being a templating landmark in arthroplasty. Indeed, the fossa, which is almost mature at 16 weeks of intrauterine development, plays a key role in hip development, enabling its nutrition through vascularization and synovial fluid, as well as the influx of chondrogenic stem/progenitor cells that build articular cartilage. The pulvinar, a fibrofatty tissue in the fossa, has the same developmental origin as the synovium and articular cartilage and is a biologically active area. Its unique anatomy allows for homogeneous distribution of the axial loads into the joint. It is composed of intra-articular adipose tissue (IAAT), which has adipocytes, fibroblasts, leucocytes, and abundant mast cells, which participate in the inflammatory cascade after an insult to the joint. Hence, the fossa and pulvinar should be considered in decision-making and surgical outcomes in hip preservation surgery, not only for their size, shape, and extent, but also for their biological capacity as a source of cytokines, immune cells, and chondrogenic stem cells. Cite this article: Bone Joint Res 2020;9(12):857-869.Entities:
Keywords: Acetabular fossa; Acetabulum; Hip joint; Intra-articular adipose tissue; Ligamentum teres
Year: 2020 PMID: 33275027 PMCID: PMC9021901 DOI: 10.1302/2046-3758.912.BJR-2020-0254.R1
Source DB: PubMed Journal: Bone Joint Res ISSN: 2046-3758 Impact factor: 4.410
Ontogeny of the acetabular fossa.
| Time of intrauterine development | Stage of development | Stage of acetabular development | Stage of fossa development | Stage of cartilage development | Molecular development |
|---|---|---|---|---|---|
| 4 weeks |
|
Differentiate from primordial mesoderm Three-layered cluster of mesenchymal tissue at the limp buds |
Derives from the inner layer Dense metachromatic tissue |
Blastematous metachromatic cells |
Chondrogenic marker expression ( Condensation of
|
| 8 weeks |
|
Creation of the joint cavity by progressive thinning of the inner layer Ligaments created |
Identifiable fossa, turning into a looser tissue Central monovascular invasion |
Some chondroid cells liberated on the periphery of the fossa |
Decrease in type II collagen expression Increase in GDF5 and BMP2 expression |
| 12 weeks |
|
Bony chondrification of the ilium, pubis, and ischium Development of labrum and rim delimitation by perichondrium |
Multivascular invasion in direction to the peripheral area Cartilaginous matrix over fossa undergoes chondrolysis |
Vessels liberating numerous cartilaginous cells at periphery of the fossa |
|
| 16 weeks |
|
Centres of ossification of the 3 pelvic bones mature Triradiate cartilage visible |
Extensive capillary network Mast cells organized in rows Superficial cells turn into synovium-like cells (pulvinar) IAAT deposit (pulvinar) |
All areas peripheral to the fossa surrounded by articular cartilage |
Increase in CD34, CD44, and CD45 |
| Last 6 months |
|
6-fold increase in size until birth |
Progressive anterior reorientation |
Progressive reorientation, positioned more posteriorly Thickening of the articular cartilage |
Proliferation of ROSACreER/R26R Confetti articular chondrocytes decreases progressively Thickening of the cartilage occurs through an increase in the volume of chondrocytes |
IAAT, intra-articular adipose tissue
Fig. 1Clinical image of the gross anatomy of a nonarthritic acetabulum from a 75-year-old male diagnosed with a right neck of femur fracture.
Fig. 2Cadaver model of the acetabulum demonstrating different shapes of acetabular fossa and articular cartilage.
Characteristics of intra-articular adipose tissue versus white adipose tissue.
| Characteristic | IAAT | WAT |
|---|---|---|
| Location | Pulvinar of the hip, Hoffa’s fat pad in the knee, lumbar facet, intermetacarpal, olecranon, and coronoid fossa | Subcutaneous, viscera, mediastinum, muscles |
| Thickness | 2.0 mm to 4.4 mm | 1.65 mm to 18 mm |
| Cellularity | Mature adipocytes, fibroblasts, macrophages and other leucocytes, mast cells, and mesenchymal stem cells | Mature adipocytes, pericytes, adipose precursor cells, leucocytes, mesenchymal progenitor cells |
| Vascularization | Rich capillaries (derived from obturator artery in case of the pulvinar) | Diverse |
| Innervation | Branches from obturator and sciatic nerves in case of the hip. Peptidergic C-fibres | Diverse. Sympathetic nerve (tyrosine hydroxylase immunoreactive (TH+) fibres |
| Most relevant cytokines produced | IL-6, IL-8, PGE2, leptin, adiponectin, resistin, adipsin, ghrelin | TNF-alpha, IL-6, IL-8, PGE2, leptin, adiponectin, resistin, adipsin, ghrelin, visfatin, chemerin, VEGF, HGF, TGF-beta, FGF |
| Role | Sensory regulation, load transmission, synovial fluid production, development and growth (in case of the acetabulum), local regulation of inflammatory response | Lipid and glucose (insulin) metabolism, coagulation, appetite and body weight regulation, reproduction and fertility, mechanical protection, temperature regulation, bone marrow metabolism, immune response modulator, systemic inflammatory response |
| Variation in gross morphology during metabolic disorders (obesity, metabolic syndrome, lipodystrophy, cachexia) | No | Yes |
| Variation in cellular composition and cytokine secretion during metabolic disorders | Yes, adopting a proinflammatory profile | Yes |
FGF, fibroblast growth factor; HGF, hepatocyte growth factor; IAAT, intra-articular adipose tissue; IL, interleukin; PGE2, prostaglandin E2; TGF, transforming growth factor; TNF, tumour necrosis factor; VEGF, vascular-endothelial growth factor; WAT, white adipose tissue.
Fig. 3Cellular and molecular changes in the pulvinar leading to osteoarthritis (OA) development. Recent studies highlighted the proinflammatory role of intra-articular adipose tissue (IAAT) in the development of OA. Our hypothesis is that these changes cause an imbalance in the differentiation of mesenchymal stem cells (MSCs), biasing towards the adipocyte lineage at the expense of the osteoblast and chondrocyte lineages. Adipokines combined with proinflammatory cytokines accumulate in the synovial fluid to further accelerate cartilage degradation and degeneration. Arrows refer to upregulation and downregulation. ACAN, aggrecan; ADAMTS-4, a disintegrin and metalloproteinase with thrombospondin motifs 4; CCL3L1, C-C motif chemokine ligand 3 like 1; COL2A1, collagen type 2 alpha 1; CXCL3, chemokine C-X-C motif ligand 3; IL, interleukin.