Agathe Genestar - Ostéopathe D.O générale et pédiatrique

18/01/2026

Hot off the Press 🔥

𝗢𝘀𝘁𝗲𝗼𝗮𝗿𝘁𝗵𝗿𝗶𝘁𝗶𝘀 𝗮𝘀 𝗮 𝘀𝘆𝘀𝘁𝗲𝗺𝗶𝗰 𝗱𝗶𝘀𝗲𝗮𝘀𝗲

Historically, osteoarthritis (OA) has been narrowly understood as an unavoidable, cartilage-centric, wear-and-tear disease that is inevitable with ageing (https://pubmed.ncbi.nlm.nih.gov/22392533/). Growing evidence from both preclinical and clinical research, however, challenges this narrow perspective. Instead, OA is increasingly understood as a systemic condition that affects the whole person, shaped by ongoing interactions between joint tissues and biological processes throughout the body (https://pubmed.ncbi.nlm.nih.gov/41339496/).

⚖️Rather than being limited to mechanical damage, OA involves a combination of disrupted cellular metabolism, breakdown of the extracellular matrix, impaired repair mechanisms, and activation of innate immune pathways. These processes are not confined to the joint itself. They are strongly influenced by broader systemic factors, including ageing, obesity, sex-specific biology, metabolic disturbances, chronic inflammation, and inter-organ communication (https://pubmed.ncbi.nlm.nih.gov/30209413/, https://pubmed.ncbi.nlm.nih.gov/31621562/, figure 1 top). This broader view also helps explain a common clinical observation: structural joint damage seen on imaging often correlates poorly with pain severity. Pain in OA appears to be shaped not only by local tissue pathology but also by central and systemic mechanisms such as pain sensitization and psychosocial influences (https://pubmed.ncbi.nlm.nih.gov/31621573/, https://pubmed.ncbi.nlm.nih.gov/30307131/).

📘 A brand-new review by Collins and colleagues (https://pubmed.ncbi.nlm.nih.gov/41339496/) emphasizes the role of adipose tissue and metabolic dysfunction as active drivers of OA, rather than passive consequences of increased joint loading. Experimental studies show that adipokines, including leptin (a satiety hormone), as well as components of the complement system, can directly promote both joint damage and pain (https://pubmed.ncbi.nlm.nih.gov/32078923/, https://pmc.ncbi.nlm.nih.gov/articles/PMC5341385/). Notably, obesity-related OA can develop even in the absence of excessive mechanical stress on the joints (https://pubmed.ncbi.nlm.nih.gov/33443201/).

💪Loss of muscle mass and conditions such as sarcopenic obesity further increase the risk of OA and contribute to functional decline, highlighting the importance of body composition rather than body weight alone (https://pubmed.ncbi.nlm.nih.gov/23312414/, https://pubmed.ncbi.nlm.nih.gov/40746030/).

💊 The authors also stress the need to move beyond a one-size-fits-all view of OA by applying phenotyping and endotyping approaches. Identifying distinct biological subtypes of OA may help explain why disease-modifying osteoarthritis drugs (DMOADs) have repeatedly failed in clinical trials (https://pubmed.ncbi.nlm.nih.gov/41339496/). Factors such as heterogeneous patient populations, treatment initiation at advanced disease stages, and an overemphasis on single tissues or pathways have likely limited therapeutic success (https://pubmed.ncbi.nlm.nih.gov/29609224/). Encouragingly, systemically acting treatments—including GLP-1 receptor agonists, metformin, and anti-inflammatory drugs originally developed for metabolic or cardiovascular conditions—are emerging as promising options for specific OA subgroups (https://pubmed.ncbi.nlm.nih.gov/39476339/, https://pubmed.ncbi.nlm.nih.gov/40179178/).

🔄 In addition to the concept that systemic factors can influence OA, there is growing evidence that shows the effects of knee pain and damage on the rest of the organism, illustrating a bidirectional relationship. This concept has also been demonstrated in studies showing that knee injury and pain might cause changes to the cardiovascular system (https://www.oarsijournal.com/article/S1063-4584(24)00059-1/fulltext) , brain (https://pubmed.ncbi.nlm.nih.gov/36593507/, https://pubmed.ncbi.nlm.nih.gov/36374499/) adipose tissue (https://pubmed.ncbi.nlm.nih.gov/40279436/) and other organ systems (figure 1, bottom). These data suggest that systemic factors can drive OA and, in turn, OA can have systemic consequences (figure)). This bidirectional relationship reinforces the idea of OA as a chronic, multi-organ condition rather than an isolated joint disorder.

07/01/2026

03/01/2026

12/12/2025

Nouveau au cabinet à Flémalle!! La thérapie par Andullation! alliée de nombreuses autres thérapies, elle agit comme un boost métabolique. Prenez le temps d'y jeter un œil, vous pourriez aimer!

07/11/2025

29/10/2025

10/10/2025

📌◼️ Understanding Modic Changes: A Key Indicator of Vertebrogenic Pain📃

✔️Modic changes are specific findings observed on magnetic resonance imaging (MRI) that are critical in the diagnostic evaluation of chronic low back pain (CLBP).
These changes relate directly to degenerative endplate changes and edema in the vertebral bodies adjacent to the intervertebral disc.

👉◼️ Modic Changes and Vertebrogenic Pain
Identifying Modic changes is crucial because they characterize vertebrogenic pain, one of the potential sources of axial chronic low back pain.

▪️ Vertebrogenic Pain: This pain etiology is characterized by the degeneration of the smooth endplate adjacent to the disc. The endplate serves as the nutrient porous barrier between the vertebral body and the disc.

▪️ Pain Transmission: The pain associated with endplate degeneration is carried by the fibers of the basivertebral nerve (BVN).

▪️ Imaging Evidence: When investigating axial CLBP, the presence of changes in the endplates, such as invaginations and edema in the vertebral bodies (specifically Modic type I–II), supports a diagnosis of vertebrogenic pain.

👉◼️ Visualizing Modic Changes on MRI
Modic changes are classified into types based on their specific signal intensity appearance on T1 and T2 weighted MRI images.

▪️ Modic type 1: Dark on T1 and bright on T2.
▪️ Modic type 2: Bright on both T1 and T2.
▪️ Modic type 3: Dark on both T1 and T2.

▪️ Modic types I and II are the types explicitly mentioned as being visible in patients experiencing vertebrogenic pain.

👉◼️ Differentiating from Other CLBP Sources
Vertebrogenic pain, indicated by Modic changes, presents as central axial pain that may radiate across the lumbar region.
It must be differentiated from other causes of axial CLBP, such as facet joint syndrome and sacroiliac joint (SIJ) pain.

▪️ In patients with discogenic pain, the endplate generally remains intact, although a high-intensity zone (HIZ) may be present within the annulus of the disc.

▪️ Vertebrogenic pain and discogenic back pain are estimated to constitute 39% of all causes of chronic low back pain.

👉◼️ Clinical Significance: Treatment
The identification of Modic changes on MRI has direct implications for treatment.

▪️ If a patient presents with axial CLBP, without radicular symptoms, and other pain generators like the facet joint and SIJ have been ruled out, the presence of degenerative endplate changes on MRI makes it prudent to consider basivertebral nerve ablation as the next course of action to help alleviate debilitating pain.

▪️ Basivertebral nerve ablation is a procedure targeting the nerve fibers that carry pain signals due to endplate degeneration.

📌Significance for physiotherapists?

👉Modic changes have important implications in physiotherapy management, as they help guide both the treatment focus and clinical expectations in patients with chronic low back pain (CLBP).

◼️ 1. Identifying the Pain Source
▪️ Modic changes indicate vertebrogenic pain, meaning the primary pain generator is the vertebral endplate, not the disc, muscle, or facet joints.
▪️ This helps physiotherapists tailor treatment away from interventions targeting discogenic or facet-related pain.

◼️ 2. Adjusting Exercise Prescription
▪️ Early stages (Modic type I, with inflammation and edema) may require load management, gentle mobility, and graded activity, avoiding excessive spinal loading that aggravates endplate stress.
▪️ Later stages (Modic type II, fatty degeneration) allow for progressive strengthening and stabilization programs focusing on trunk endurance, posture control, and functional reconditioning.

◼️ 3. Pain Education and Expectation Setting
▪️ Patients with Modic changes often experience chronic, central low back pain that can persist despite traditional soft tissue–based therapy.
▪️ Educating the patient that their pain has a vertebrogenic origin helps set realistic expectations and reinforces the importance of consistent, long-term management.

◼️ 4. Multidisciplinary Approach
▪️ Recognition of Modic changes signals when collaboration with pain specialists or spine physicians may be beneficial.
▪️ If pain remains refractory to conservative physiotherapy, the patient may be a candidate for basivertebral nerve ablation, while physiotherapy continues to address movement control and functional restoration post-procedure.

◼️ 5. Clinical Insight in Imaging Interpretation
▪️ Understanding Modic changes enables physiotherapists to interpret MRI findings more meaningfully, linking imaging to functional deficits and guiding evidence-informed rehabilitation planning.

10/10/2025

✅ 📃Revealing the complexity of meniscus microvasculature through 3D visualization and analysis

◼️ Background and Motivation
💠 The meniscus is crucial for knee joint health and functionality, and its vascular supply is key to its healing potential.
💠 Tears in vascularized areas (Red-Red zones) can promote tissue healing due to the supply of oxygen and nutrients, while damage in avascular areas (White-White zones) often fails to repair.
💠 Historically, the study of meniscal vascularity has relied primarily on two-dimensional (2D) imaging techniques, making a comprehensive 3D understanding essential.

👇

◼️Methodology
🔹 The study aimed to investigate the feasibility of mapping and visualizing the microvasculature within the human meniscus using advanced 3D imaging techniques, as well as analyzing the network's regional characteristics via quantitative parameters.

▪️ Sample Preparation
🧪 Samples consisted of six menisci from three Thiel-fixated human cadaver legs (male donors, mean age 75).

▪️ Contrast Agent Injection
💉 A polymerizing contrast agent, μAngiofil, was injected through the cannulated femoral artery.
💧 Prior to contrast injection, a low-viscosity silicone oil with blue dye was perfused to flush out postmortem clots and restore flow.

▪️ Micro-CT Imaging

📸 Micro-CT analysis was performed at three gradually increasing spatial resolutions:

Group A (low resolution, 60 μm voxel size)

Group B (medium resolution, 30 μm voxel size)

Group C (high resolution, 15 μm voxel size)

▪️ 3D Quantitative Analysis
🧮 The vascular network was segmented using a combination of the Max Entropy algorithm and the white top-hat operation to capture both large vessels and finer details.
📊 Quantitative parameters, including diameter, length, tortuosity, and branching patterns, were assessed in a zone-based analysis.
🩻 The menisci were divided into four radial portions (anterior, mid-anterior, mid-posterior, and posterior) and four circumferential zones (perimeniscal (PM), zone 1 (RR), zone 2 (RW), and zone 3 (WW)).

👇

◼️ Key Findings

▪️ Vascular Distribution (Circumferential Zones)
🩸 The outer perimeniscal zone exhibited the highest vascular volume contribution, containing more than 72% of the blood vessels in both the lateral and medial menisci.
🩸 When excluding the perimeniscal area, zone 1 (RR) displayed the highest vascular volume.
🩸 The contribution of zone 3 (WW, the innermost third) to the overall meniscal vasculature was less than 5% in the lateral meniscus and less than 2.5% in the medial meniscus.

▪️ Vascular Distribution (Radial Zones)
🧠 In the lateral meniscus, the majority of vessels (68%) were found in the mid-anterior and posterior zones.
🧠 In the medial meniscus, the anterior, mid-anterior, and posterior regions contained over 80% of the total vessel volume.
🧠 In both menisci, the mid-posterior portion showed the lowest contribution to the overall vasculature.

▪️ Vascular Parameters
📈 Variations in vascular parameters were found between the different circumferential and radial meniscal zones.
📈 The vascular segments of the perimeniscal zone had a significantly different diameter compared to the other circumferential zones in both menisci.
📈 The vascular network showed a zone-dependent structure and organization in the radial portions.

▪️ Resolution Importance
🔍 The study emphasized the importance of spatial resolution.
🔍 Analysis performed at higher resolutions (Groups B and C) allowed for the identification of a greater number of vascular segments and nodes compared to the low-resolution scan (Group A).
🔍 Higher resolution analysis also enabled the detection of smaller vessels, resulting in a lower average diameter value in Groups B and C.

👇

◼️ Significance

🌐 The main strength of this work is the 3D non-destructive visualization and quantification of blood vessels, which is an improvement over older, destructive methods like serial sectioning and vascular corrosion casting.
🩺 The ability to perform a detailed study of vascular morphology and topology could be a valuable method to evaluate the arteriogenic and angiogenic response to meniscal repair surgery.

💡 The findings, both from this study and future research using this technique, are expected to improve the understanding of microvascular distribution, potentially leading to improved therapeutic strategies.

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⚠️Disclaimer: Sharing a study or a part of it is NOT an endorsement. Please read the original article and evaluate critically.⚠️

Link to Article 👇

02/10/2025

📘 A Clinician's Guide to Triangular Fibrocartilage Complex (TFCC) Tears: Assessment and Management

◼️ The Triangular Fibrocartilage Complex (TFCC) tear is one of the most common causes of ulnar-sided wrist pain and disability, frequently presenting in physiotherapy clinics
◼️ A thorough understanding of the TFCC's intricate anatomy, biomechanics, and the evidence-based management pathways is essential for effective patient care
◼️ This post provides a detailed overview for clinicians, covering assessment, classification, and management strategies based on current evidence

🦴 Anatomy and Biomechanics: The Keystone of the Ulnar Wrist

◼️ The TFCC is a robust ligamentous structure with two primary functions: it stabilizes the distal radioulnar joint (DRUJ) and acts as a shock absorber between the ulnar head and the carpus

Key Anatomical Components:
◼️ The central component is the triangular fibrocartilage (articular disk)
◼️ Supported by volar and dorsal radioulnar ligaments, the volar ulnotriquetral and ulnolunate ligaments, the ulnar collateral ligament, and the extensor carpi ulnaris (ECU) tendon sheath
◼️ The TFCC attaches radially to the distal radius, a relatively avascular zone with poor healing potential
◼️ It attaches ulnarly to both the ulnar fovea (proximal lamina) and the ulnar styloid (distal lamina). This peripheral region is well-vascularized, giving it good healing potential

Biomechanics and Ulnar Variance:
◼️ The TFCC is a key static stabilizer of the DRUJ, with dynamic stability contributed by the ECU and pronator quadratus muscles
◼️ Load transmission across the wrist is heavily influenced by ulnar variance—the relative length of the ulna to the radius
◼️ With neutral ulnar variance, the ulnocarpal joint transmits about 18% of the axial load
◼️ With a 2.5 mm positive ulnar variance, this load increases to 42%, making the thinner TFCC more prone to degenerative tears
◼️ With a 2.5 mm negative ulnar variance, the load decreases to just 4.3%

🩺 Etiology and Classification

◼️ TFCC tears can be traumatic (acute) or degenerative (chronic)

Traumatic Tears (Palmer Type 1):
◼️ Often caused by a fall onto an outstretched hand (FOOSH), a violent forearm twist, or axial loading
◼️ Classified by the location of the tear (central, radial, or ulnar avulsion)

Degenerative Tears (Palmer Type 2):
◼️ Result from chronic overload, often associated with ulnocarpal impaction syndrome and positive ulnar variance
◼️ Graded by the severity of wear, from chondromalacia to full perforation and arthritis

Treatment-Oriented Classification:
◼️ Atzei, Luchetti, and Garagnani further refine Palmer 1B tears based on tear repairability and DRUJ stability, guiding surgical decision-making

🧾 Clinical Assessment: From History to Provocative Testing

◼️ A definitive diagnosis relies on a combination of thorough history, physical examination, and imaging

Subjective Assessment:
◼️ Patients typically report ulnar-sided wrist pain, sometimes with clicking or popping with forearm rotation, decreased grip strength, and a sensation of instability
◼️ Traumatic tears have a clear mechanism of injury
◼️ Degenerative tears often have an insidious onset

Objective Examination:
◼️ Always include comparison to the unaffected side
◼️ Observation: Look for bony asymmetry or dorsal prominence of the ulna, which can indicate DRUJ injury
◼️ Palpation: Tenderness over the fovea (between ulnar styloid, FCU tendon, and pisiform) = positive ulnar fovea sign, may indicate foveal disruption of the TFCC
◼️ Sensitivity 73-90%, specificity 8-44%
◼️ Range of Motion & Strength: Passive forearm rotation often elicits pain and mechanical symptoms, resisted rotation may reveal weakness
◼️ Provocative Maneuvers: Integral for reproducing symptoms and assessing stability

Ballottement Test: Assesses DRUJ instability by translating the ulna in volar/dorsal directions; increased translation = instability

Press Test: Patient lifts from chair using arms; focal ulnar wrist pain = positive

Grind Test: Axial compression + forearm rotation; pain/crepitus may indicate arthritis or instability. Sensitivity 90-93%, specificity 12-20%

Imaging:
◼️ Plain x-rays rule out fractures and assess ulnar variance (cannot visualize TFCC tear itself)
◼️ MRI/MRA detail soft-tissue injuries (MRA higher accuracy)
◼️ Arthroscopy = gold standard for definitive diagnosis, allows visualization and assessment of size, location, and repairability

⚕️ Management Strategies: From Conservative Care to Surgical Intervention

Conservative Management:
◼️ Initial management for most TFCC tears is non-operative
◼️ Immobilization: Splint/cast for 4-6 weeks. Resolves symptoms in about 60% of patients
◼️ Activity modification & Anti-inflammatories
◼️ Corticosteroid Injection: Considered if symptoms persist after immobilization

Surgical Management:
◼️ Indicated if conservative measures fail
◼️ Tailored to tear type, location, and chronicity

Arthroscopic Debridement: For stable, central (avascular) tears (Palmer 1A)

Arthroscopic/Open Repair: For peripheral tears in vascular zone (Palmer 1B). Includes suturing or reattaching TFCC to restore DRUJ stability

Reconstruction: For irreparable or chronic tears; tendon graft (often palmaris longus) used

Ulnocarpal Unloading Procedures: For degenerative tears with positive ulnar variance → ulnar shortening osteotomy or wafer procedure

Salvage Procedures: For severe DRUJ arthritis → Darrach, Sauve-Kapandji, or arthroplasty

🏋️ Post-Operative Rehabilitation Considerations

◼️ Following Debridement: ~2 weeks cast immobilization
◼️ Following Repair: ~6 weeks cast immobilization → progressive rehab → return to sport at 3 months
◼️ Following Reconstruction: Up to 12 weeks immobilization (long-arm cast → splints). Supervised ROM begins ~3 weeks post-op
◼️ Electroacupuncture + standard rehab after arthroscopic repair may improve hand function (DASH score)

📊 Prognosis and Key Takeaways

◼️ Prognosis depends on:

1. Vascularity: Peripheral (ulnar) portion heals well; central & radial portions avascular, poor healing

2. Chronicity: Acute tears (6 months) have poor healing

◼️ For physiotherapists: success depends on accurate diagnosis, understanding underlying pathology, knowledge of surgical procedures, and managing post-op rehab
◼️ Managing patient expectations regarding healing times and functional outcomes is paramount

29/09/2025

Your Muscles and Brain Are Talking. Exercise Is the Conversation Starter! 🧠💪

▪️ Ever feel sharper and more focused after a good workout? It’s not just a feeling—it’s science! There’s a powerful, two-way communication system in your body called muscle-brain crosstalk

▪️ Here’s how it works in 3 simple steps:
💡 You Move: When you exercise, your muscles get to work. Whether it's walking, swimming, or lifting weights, this activity is the trigger.
📩 Muscles Send Messages: In response to exercise, your muscles release special messenger molecules called myokines into your bloodstream. Think of them as tiny health-boosting packages sent directly from your muscles!
🧠 Your Brain Benefits: These myokines travel to your brain and deliver incredible benefits, such as:
▪️ Protecting brain cells and helping to create new ones
▪️ Improving memory and cognitive function
▪️ Fighting inflammation in the brain, which is linked to aging and disease
▪️ Helping prevent age-related diseases like sarcopenia (muscle loss) and cognitive decline, including Alzheimer's disease

▪️ It’s a positive feedback loop! As your brain gets healthier from these messages, it becomes better at controlling your muscles, which helps them stay strong and release even more beneficial myokines

▪️ Ready to get the conversation started?
🏃 You don’t have to run a marathon! Research suggests that for older adults, aiming for low- to moderate-intensity aerobic exercise (like brisk walking) 3 times a week for 12 weeks or more can significantly boost myokine levels and support brain health.
🏋️ Resistance training 2-3 times a week is also highly effective

▪️ So next time you exercise, remember you’re not just strengthening your body—you’re sparking a vital conversation that keeps your brain young and healthy!

Link to Article👇👇

14/08/2025