How Micro-Fragmented Fat Tissue May Calm Joint Inflammation
Francesca Paolella, Cristina Manferdini, Elena Gabusi, Laura Gambari, Giuseppe Filardo, Elizaveta Kon, Erminia Mariani, Gina Lisignoli · Journal of Cellular Physiology · 2018
Lab Study Shows Fat Tissue Reduces Inflammatory Signals
Osteoarthritis (OA) causes ongoing inflammation in your joints. This inflammation involves immune cells called macrophages in the joint lining. These cells release chemical signals that break down cartilage and cause pain. Italian researchers wanted to understand how micro-fragmented adipose tissue (MFAT)—specially processed fat from your own body—might calm this harmful process.
This laboratory study tested MFAT against inflamed joint cells taken from OA patients. The goal was to see if MFAT could reduce the inflammatory signals these cells produce.
MFAT Lowers Key Chemicals That Attract Damaging Cells
The researchers found that MFAT significantly reduced two important inflammatory signals:
CCL2/MCP-1: A chemical that attracts destructive immune cells to the joint
CCL3/MIP-1α: Another signal that draws macrophages into inflamed tissue
By lowering these signals, MFAT may help reduce the flood of damaging cells into arthritic joints. This could slow the cycle of inflammation that worsens OA over time.
Fat Tissue Outperforms Isolated Stem Cells in Some Ways
The study compared two approaches: whole micro-fragmented fat tissue (MFAT) versus stem cells removed from that tissue (called MF-ADMSCs). Interestingly, the complete MFAT worked better than isolated stem cells for several measures.
MFAT reduced more inflammatory markers than stem cells alone. This suggests the natural structure of fat tissue matters. The complete tissue contains a supportive network of blood vessels and helper cells called pericytes. These work together in ways that isolated cells cannot match.
Protective Enzyme Blocker Increases with Treatment
The study measured MMP-9, an enzyme that breaks down cartilage. MFAT reduced MMP-9 levels in the inflamed joint cells. Even more promising, MFAT increased TIMP-1—a natural substance that blocks harmful enzymes like MMP-9.
Think of MMP-9 as scissors cutting your cartilage. TIMP-1 acts like a protective cover for those scissors. By increasing TIMP-1, MFAT may help protect your cartilage from ongoing damage.
Research Reveals How MFAT "Switches Off" Inflammation
The researchers discovered the biological pathway MFAT uses to calm inflammation. MFAT reduced a receptor called TLR4 and lowered activity in the NFκB pathway. These are like alarm systems that trigger inflammation in your body.
When these pathways are overactive, they keep inflammation going. By turning down these signals, MFAT may help break the cycle of chronic joint inflammation.
What This Means for Your Treatment Decision
This laboratory study provides scientific evidence for how MFAT may work inside arthritic joints. The findings suggest MFAT could:
Reduce signals that attract damaging immune cells
Protect cartilage by blocking harmful enzymes
Calm the inflammation pathways that drive OA symptoms
Keep in mind this was a laboratory study, not a clinical trial in patients. The inflamed cells came from real OA patients, which makes the model relevant. However, results in a laboratory dish may differ from results in a living joint.
The research supports the idea that Lipogems® treatment preserves the natural healing structure of fat tissue. This complete tissue appears more effective than isolated stem cells for reducing certain inflammatory markers.
If you are considering Lipogems® for OA, this study adds to the scientific understanding of how the treatment may work. Ask your doctor how these findings relate to your specific condition and treatment goals.
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Source: Paolella et al., Journal of Cellular Physiology, 2018.
Original Publication
Effect of microfragmented adipose tissue on osteoarthritic synovial macrophage factors
Francesca Paolella, Cristina Manferdini, Elena Gabusi, Laura Gambari, Giuseppe Filardo, Elizaveta Kon, Erminia Mariani, Gina Lisignoli · Journal of Cellular Physiology · 2018
This study investigated the mechanisms of action of microfragmented adipose tissue (MF) and MF-derived adipose mesenchymal stromal cells (MF-ADMSCs) on inflammatory osteoarthritic (OA) synoviocytes. MF represents an innovative one-step approach to obtain adipose-derived cells while avoiding extensive cell expansion procedures. The researchers examined the production of inflammatory factors, chemokines, and matrix metalloproteinases by MF and MF-ADMSCs, both alone and in coculture with OA synoviocytes. Results showed that MF produced low levels of inflammatory factors (IL-6, CCL5/RANTES, CCL2/MCP-1, CCL3/MIP-1α) and matrix metalloproteinase 9 (MMP-9) but higher levels of CXCL8/IL-8 compared to MF-ADMSCs. In coculture, MF increased synoviocyte metabolic activity and IL-6 release but significantly reduced macrophage-specific chemokines (CCL2/MCP-1, CCL3/MIP-1α) and MMP-9. Additionally, MF increased TIMP-1 (MMP-9 inhibitor) and down-regulated toll-like receptor 4 (TLR4) and NFκB signaling pathways. The findings demonstrate that MF exhibits distinct effects from MF-ADMSCs on inflamed synoviocytes, particularly in reducing macrophage markers and activity through modulation of TLR4 and NFκB signaling, suggesting potential therapeutic applications for OA treatment.