Usługi Medyczne - Fizjoterapia Dominik Miły

20/03/2025

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Hot off the Press 🔥

Does Leptin and Insulin Levels Influence Pain and Disability in Subjects With Frozen Shoulder?

🙋 Frozen shoulder (FS), also known as adhesive capsulitis, is characterised by unexplained stiffness, limited mobility, and pain in the shoulder joint. Its aetiology can be classified as either primary, with no identifiable cause, or secondary to underlying conditions (https://pubmed.ncbi.nlm.nih.gov/33312703/; https://pmc.ncbi.nlm.nih.gov/articles/PMC8144309/). Recognised risk factors for FS include diabetes, Dupuytren's syndrome, nephrolithiasis, Parkinson's disease, shoulder trauma, smoking, cancer, cardiovascular or cervical surgery, and chronic regional pain syndrome. Many of these risk factors are associated with fibroblastic and inflammatory processes and insulin resistance (https://pubmed.ncbi.nlm.nih.gov/38617059/). FS affects an estimated 2% to 5% of the general population, with a notably higher prevalence in individuals aged 40 to 60 years and being more commonly observed in women than in men (https://pmc.ncbi.nlm.nih.gov/articles/PMC9605091/).

👉 Leptin, a peptide hormone from adipose tissue, regulates energy balance and has proinflammatory properties, while insulin resistance, often assessed via HOMA, is linked to metabolic dysregulation. Both are implicated in inflammatory and fibroblastic processes in musculoskeletal disorders (https://pmc.ncbi.nlm.nih.gov/articles/PMC9605091/, https://pubmed.ncbi.nlm.nih.gov/35406000/), raising the hypothesis that they may influence FS symptoms

📘 A brand-new study by Pérez-Montilla, published in the “European Journal of Pain” explores their association with pain, disability, and ROM in FS patients. (https://pubmed.ncbi.nlm.nih.gov/40067138/)

✅ Materials and Methods

👫 Participants: 34 patients (9 men, 25 women, aged 18–60) with primary FS, recruited from a clinic in Cordoba. Inclusion required a diagnosis of FS for at least 3 months; exclusion criteria included systemic diseases or neurological conditions.

✅ Outcome Measures:

▶️ Shoulder Pain and Disability Index (SPADI): Assesses pain (5 items) and disability (8 items), scored out of 100, with higher scores indicating worse outcomes.

▶️ Shoulder ROM: Measured with a goniometer for flexion, extension, abduction, adduction, and internal/external rotation.

▶️ Metabolic Biomarkers: Blood samples analyzed for leptin and insulin levels; HOMA calculated from fasting glucose and insulin to assess insulin resistance.

🔑 Key Findings:

▶️ Higher leptin levels were significantly associated with:

👉 Increased SPADI pain scores (R² = 0.114, p = 0.005)
👉Increased SPADI disability scores (R² = 0.110, p = 0.006)
👉 Reduced shoulder flexion (R² = 0.074, p = 0.025)

▶️ Higher insulin resistance (HOMA) was significantly associated with:

👉 Increased SPADI pain scores (R² = 0.096, p = 0.010)
👉 Increased SPADI disability scores (R² = 0.081, p = 0.017)
👉 Reduced shoulder flexion (R² = 0.061, p = 0.028)

✅ Discussion

▶️ FS is much more than a mechanical problem. The study confirms that elevated leptin and insulin resistance are associated with worse pain, disability, and reduced shoulder flexion in FS patients, suggesting a role for metabolic and inflammatory pathways in FS. Leptin’s pro-inflammatory effects may exacerbate pain and fibrosis, consistent with its role in other conditions like osteoarthritis (https://pubmed.ncbi.nlm.nih.gov/25002656/). However, conflicting evidence (e.g., lower leptin in shoulder stiffness by Ko et al., https://pmc.ncbi.nlm.nih.gov/articles/PMC9605091/) suggests context-dependent effects. This discrepancy could reflect leptin's complex, dual nature, where it may exert either pro-or anti-inflammatory effects depending on the disease stage and context.

✅ Therapeutic Implications: Lifestyle interventions targeting leptin and insulin resistance—e.g., high-intensity exercise (https://pubmed.ncbi.nlm.nih.gov/38015889/), intermittent fasting, ketogenic/Mediterranean diets, or green tea—could complement traditional FS treatments like traditional movement based therapies (https://pubmed.ncbi.nlm.nih.gov/35682282/, https://pubmed.ncbi.nlm.nih.gov/30865775/, https://pubmed.ncbi.nlm.nih.gov/35750605/).

▶️ Furthermore, as psychological factors play a significant role in frozen shoulder (FS), influencing both symptom severity and underlying disease mechanisms, these results stress the importance of a biopsychosocial understanding of FS. A systematic review by Brindisino et al. (https://pubmed.ncbi.nlm.nih.gov/37867399/) found that pain-related fear, depression, and anxiety can predict disability levels, pain intensity, and recovery duration in FS patients. Additionally, research suggests that chronic psychosocial stress may contribute to FS by disrupting metabolic and immune processes. Navarro-Ledesma et al. (https://pubmed.ncbi.nlm.nih.gov/38617059/) proposed that prolonged emotional stress, combined with immune system challenges, may drive the inflammation and fibrosis seen in FS. These findings highlight the importance of considering psychological well-being in FS treatment and management.

▶️ The addressed strategies may reduce inflammation and improve metabolic health, potentially alleviating symptoms. Further studies are needed to provide empirical evidence for these strategies.

📸 Illustration: Structural changes during frozen shoulder, Millar et al. (2022, https://pubmed.ncbi.nlm.nih.gov/36075904/)

a | The healthy capsule is collagenous in structure, composed primarily of dense type I collagen and elastic fibre bundles with limited blood vessels and nerve fibres. The main cell type within this membrane is the fibroblast, which maintains capsule health by producing extracellular matrix (ECM) proteins that provide a supportive yet flexible structure.

b | In frozen shoulder, there is fibrosis and thickening of the connective tissue membrane as well as the adjacent synovial membrane.

c | Fibroproliferation results in an increased number of fibroblasts producing more ECM proteins, resulting in a dense and poorly organized fibrillar structure. These fibrotic changes are accompanied by inflammation, neoangiogenesis and neoinnervation. The consequence is a reduced joint volume and increased stiffness of the capsule, causing restricted movement and pain.

22/03/2024

Neurogenic scapular Winging💡

👉Neurogenic scapular winging is a rare, but potentially debilitating condition that can affect the ability to lift, pull, and push heavy objects, as well as to perform daily activities of living, such as brushing one’s hair and teeth and carrying grocery bags. (https://pubmed.ncbi.nlm.nih.gov/8549212/)

👉Most cases are due to lesions of the long thoracic and spinal accessory nerves that innervate the serratus anterior and trapezius muscles, respectively. Rarely, it may also be due to a lesion to the dorsal scapular nerve that innervates the rhomboid muscles. (https://pubmed.ncbi.nlm.nih.gov/19468892/)

👉 These scapular muscles contribute to keeping the medial border of the scapula protracted against the posterior thoracic wall, and denervation or paralysis of any of these muscles results in the winging of the medial border of the scapula as it lifts off the thoracic wall. In addition, the scapula may translate medially or laterally along the posterior thoracic wall due to unopposed muscle contraction of the other functioning scapular muscles, a distinction known as medial (serratus anterior paralysis) or lateral (trapezius or rhomboid paralysis) winging.

🙋 In medial winging (injured nerve: long thoracic, serratus anterior palsy), the entire scapula is displaced more medial and superior. The classical wall push-up tests to demonstrate medial scapula border winging (s. Illustration) seems to be less accurate than the shoulder flexion resistance test (SFRT). The SFRT is performed by resisting shoulder flexion while the elbow is fully extended with the shoulder passively positioned in 30°, 60°, and 100° flexion. A positive SFRT is defined as scapular winging. (https://pubmed.ncbi.nlm.nih.gov/36081701/)

🙋‍♂️ In lateral winging (injured nerve: Spinal accessory, cranial nerve XI, trapezius and sternocleidomastoid), the superior scapula angle is displaced more lateral and inferior. There is weakness in shoulder abduction and external rotation. (https://pubmed.ncbi.nlm.nih.gov/19468892/)

👉T he long thoracic nerve may be damaged by acute brachial neuritis, mechanical factors, and surgical procedures, including mastectomy or thoracotomy. Occasionally, patients present with bilateral scapular winging. This is most commonly related to facioscapulohumeral muscular dystrophy because it is unusual to have bilateral long thoracic nerve palsies.

👉 Similarly, rhomboid paralysis tends to be primarily neurogenic in nature. An entrapment injury of the dorsal scapular nerve is the most common cause of injury reported in the literature (https://pubmed.ncbi.nlm.nih.gov/750930/, https://mednexus.org/doi/10.5555/cmj.0366-6999.108.08.p582.01), although the site of entrapment is not well known. In addition to entrapment syndromes, direct injury to the nerve (i.e. anterior shoulder dislocation, https://pubmed.ncbi.nlm.nih.gov/2075821/) has been reported to cause rhomboid paralysis.

Illustration: https://shop.elsevier.com/books/the-netter-collection-of-medical-illustrations-nervous-system-volume-7-part-ii-spinal-cord-and-peripheral-motor-and-sensory-systems/jones-jr/978-1-4160-6386-5

19/01/2024

Tendon structure in health and disease 🦶

💡 Summary based on Scott (2015, https://pubmed.ncbi.nlm.nih.gov/26390273/)

👉 The classic description of the tensile load-bearing region of tendon includes 3 main components:

1️⃣ type I collagen fibers (70–80% of the dry weight of the tendon and represents almost 95% of the total collagen. Other collagens include collagen types II, III, IV, V, VI, IX, X, XII, and XIV) longitudinally oriented;

2️⃣ a well-hydrated, noncollagenous extracellular matrix (rich in glycosaminoglycans); and

3️⃣ cells. The predominant cell population in healthy tendon is traditionally categorized as collagen-producing fibroblasts, responsible for the synthesis of the collagen fibers and extracellular matrix. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2505234/ https://pubmed.ncbi.nlm.nih.gov/26390273/)

👉 Prominent features of chronic tendinopathy histopathology (FIGURE 1) include the following:

▶︎ a disorganization of collagen fibers,

▶︎ an increase in the number of vessels and sensory nerves, https://pubmed.ncbi.nlm.nih.gov/17604979/, https://pubmed.ncbi.nlm.nih.gov/23609815/, https://pubmed.ncbi.nlm.nih.gov/15958764/

▶︎ an increase in the hydrated components of the extracellular matrix, https://research.monash.edu/en/publications/human-tendon-overuse-pathology-histopathologic-and-biochemical-fi

▶︎ a breakdown of tissue (tendon/endotendon/paratendon) organization, (https://search.worldcat.org/de/title/human-tendons-anatomy-physiology-and-pathology/oclc/35103208) and

▶︎ haphazardly arranged proliferation of smaller, type III collagen fibers. (https://pubmed.ncbi.nlm.nih.gov/24571576/, https://pubmed.ncbi.nlm.nih.gov/12867575/)

👉There are frequently areas of cell death (eg, hypocellularity, https://pubmed.ncbi.nlm.nih.gov/16567784/) or, alternatively, of fibroblast reaction (eg, hypercellularity with rounded tenocytes and adhesions, https://pubmed.ncbi.nlm.nih.gov/3071152/).

📌 Indeed, it is typical to find both degenerative and reactive changes within the same biopsy, even in very severe, long-standing cases. It is also postulated that there is a resident population of fibroblast-like cells within tendons that, after injury, can differentiate into several lineages (osteoblast, chondrocyte, adipocyte, tenocyte), leading to metaplasia (eg, bony, cartilaginous, or adipocyte transformation, https://pubmed.ncbi.nlm.nih.gov/12837285/). Metaplasia is not usually discernible on imaging, unless the ossification is advanced, but is frequently encountered in biopsy specimens (reviewed in Lui, https://pubmed.ncbi.nlm.nih.gov/23671126/).

👉 The implication is that patients with chronic symptoms and evidence of structural change on imaging typically have profound underlying abnormalities that will not be quickly resolved, and that are associated with the loss of tendon function.

✅ At the cellular level, several authors have reported increased numbers of leukocytes (especially macrophages and mast cells) in chronically painful tendons (rotator cuff, patellar and Achilles tendons, https://pubmed.ncbi.nlm.nih.gov/24096896/, https://pubmed.ncbi.nlm.nih.gov/25081311/, https://pubmed.ncbi.nlm.nih.gov/20595553/, https://pubmed.ncbi.nlm.nih.gov/15958764/) as well as increased numbers of vascular cells (endothelial and smooth muscle, https://pubmed.ncbi.nlm.nih.gov/18067512/).

🔥 However, compared to the more immune-driven pathologies, such as rheumatoid arthritis, with measurable systemic inflammation, the number of leukocytes is small. In other words, there is indeed an inflammatory reaction within chronically painful tendinopathy, but to a lesser extent than that of immune-driven rheumatological disorders.

✅ Macrophages with accumulations of hemosiderin in their cytoplasm are more prevalent in tendinopathic than in normal tendon (https://pubmed.ncbi.nlm.nih.gov/9174456/); hemosiderin is an indicator of prior injury that resulted in an activation of the innate immune response. At a biochemical level, the cells in painful tendons produce increased levels of glycosaminoglycan and inflammatory mediators such as substance P and prostaglandin E2 (PGE2, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5714045/, https://pubmed.ncbi.nlm.nih.gov/24563019/, https://pubmed.ncbi.nlm.nih.gov/12072760/, https://pubmed.ncbi.nlm.nih.gov/9820287/).

✅ Substance P is released by peripheral sensory nerves (https://pubmed.ncbi.nlm.nih.gov/21678472/) and repetitively stretched tendon fibroblasts (https://pubmed.ncbi.nlm.nih.gov/21625050/, https://pubmed.ncbi.nlm.nih.gov/22069500/), and activates local mast cells that may contribute to pain and fibrosis (https://pubmed.ncbi.nlm.nih.gov/22343473/). Tendon cells derived from tendinopathic tendon produce more PGE2 than cells from healthy individuals, indicating a chronic upregulation (https://pubmed.ncbi.nlm.nih.gov/12072760/).

📣 Taken together, the evidence suggests that during the rehabilitation process, any worsening of edema, morning stiffness, or delayed-onset pain should be closely monitored and controlled, as inflammation could drive the tendon further down the pathological path. An early return to sport before adequate tendon load-bearing capacity is a significant risk factor for recurrence of Achilles tendinopathy (https://pubmed.ncbi.nlm.nih.gov/23770660/).

📷 Illustration:
Pereira, H. et al. (2023). Foot and Ankle Tendinopathies. In: Longo, U.G., Denaro, V. (eds) Textbook of Musculoskeletal Disorders. Springer, Cham. https://doi.org/10.1007/978-3-031-20987-1_59
https://link.springer.com/chapter/10.1007/978-3-031-20987-1_59

06/01/2024

🎊🌲Between the years, we traditionally present our "Best-of series" of the most influential posts of 2023.

📣 today 🥇 #2

Mechanisms of resorption in lumbar disc herniation

👉 Clinically, the phenomenon of spontaneous shrinkage or disappearance of a herniated lumbar IVD without surgical intervention is called reabsorption.
👉 The spontaneous resorption rate of lumbar disc herniation (LDH) is over 60% according to a meta-analysis by Zhong et al. (2017) and Chiu et al. (2015) https://pubmed.ncbi.nlm.nih.gov/28072796/, https://pubmed.ncbi.nlm.nih.gov/25009200/ with extrusion and sequestration being more prone to regression than other types. https://pubmed.ncbi.nlm.nih.gov/24630494/
But how does this actually happen? 🤓
👉 Resorption of the intervertebral disc tissue can be explained by 3 theories, but the exact mechanism is not conclusively understood:

1. Reduction in disc material size due to gradual dehydration and shrinkage, which could explain the decrease in the signal of the disc on MRI. https://pubmed.ncbi.nlm.nih.gov/11901758/
https://pubmed.ncbi.nlm.nih.gov/11750011/

2- The tension on the posterior longitudinal ligament causes the herniated disc fragment to be retracted back into the intervertebral disc space. This can be a mechanism when the annulus fibrosus (AF) is not damaged, but not with extruded and migrated fragments.
https://pubmed.ncbi.nlm.nih.gov/24316264/
https://pubmed.ncbi.nlm.nih.gov/3875236/

3. The third theory, the most well studied and with the best clinical evidence, is gradual resorption of the disc material by enzymatic degradation and phagocytosis induced by an inflammatory response and neovascularisation.

When protruding IVD tissue squeezes out of the epidural space, it disrupts immune privilege, triggering an autoimmune response, then lymphocytes activate macrophages.

Related factors secreted by IVD cells and macrophages further drive the recruitment of macrophages to the intervertebral disc in paracrine and autocrine forms. Macrophages undergo differentiation from M1 to M2 types.

M1-type macrophages secrete pro-inflammatory factors to initiate angiogenesis, promote the expression of matrix metalloenzymes and apoptosis of herniated IVD nucleus pulposus cells.

M2-type macrophages secrete anti-inflammatory factors to relieve pain response, promote new blood vessel formation, and are responsible for tissue remodeling and repair, and absorb the protruding debris to reduce the total volume of the intervertebral disc, and reduce the mechanical compression of the nerve. Throughout the process, infiltration and activation of macrophages mediate inflammatory responses, matrix metalloenzyme activation, and neovascularization.

https://pubmed.ncbi.nlm.nih.gov/16688039/
https://pubmed.ncbi.nlm.nih.gov/19333096/
https://pubmed.ncbi.nlm.nih.gov/15626982
https://pubmed.ncbi.nlm.nih.gov/35999644/

06/01/2024

Hot off the press in „BJSM” 🔥

💡 Contexts, behavioural mechanisms and outcomes to optimise therapeutic exercise prescription for persistent low back pain: a realist review

🏋️‍♀️ Therapeutic exercises are a core treatment for low back pain (LBP), but it is uncertain how rehabilitative exercise facilitates change in outcomes. Realist reviews explore how the context (C) of certain settings or populations and underlying mechanisms (M) create intended or unintended outcomes (O).

🔝 In a brand new review Wood and colleagues explored the behavioural mechanisms by which therapeutic exercise creates change in outcomes of adherence, engagement and clinical outcomes for patients with LBP. https://bjsm.bmj.com/content/early/2024/01/03/bjsports-2023-107598

📊 Of 522 initial papers identified, 75 papers were included to modify and test CMO configurations. The authors found that the patient–clinician therapeutic consultation builds a foundation of trust and was associated with improved adherence, engagement and clinical outcomes, and that individualised exercise prescription increases motivation to adhere to exercise and thus also impacts clinical outcomes. Provision of support such as timely follow-up and supervision can further facilitate motivation and confidence to improve adherence to therapeutic exercises for LBP.

📌 Engagement with, adherence to and outcomes following therapeutic exercise prescription might be optimised when the mechanisms of trust, motivation and confidence are activated. The therapeutic alliance and development of rapport are foundational to the development of trust, and facilitate holistic assessment, and identification of individual needs and beliefs. Exercise that is tailored to the individual’s goals, with personalised advice and education to reassure and build confidence, increases motivation to adhere to exercise. Timely follow-up, the perception of benefit and support from peers and from supervision can further facilitate motivation to adhere to exercise prescription, and these positively impact clinical outcomes (s. figure)

📸 Figure: Therapeutic exercise prescription affects change in outcomes of importance for those with persistent low back pain In this figure, each theme of the programme theory is represented by a circle therapeutic consultation is green, provision of support is orange and exercise specific considerations in blue) with subthemes in boxes within. Where these circles intersect, the outcomes of adherence, engagement and clinical outcomes are optimised, and the mechanisms of trust, motivation and confidence (in yellow) support the translation of the contexts into outcomes.

15/12/2023

22/10/2023

15/10/2023

Some interesting facts around the Facet joint 💡

👉 The highly innervated, diarthrodial zygapophysial joint, or the facet joint, is located at either side of the posterior vertebral body. The facet joint’s opposing bony surfaces are covered by a layer of hyaline articular cartilage (thickness: ∼0.5 mm), and the joint is encapsulated by the synovium and fibrous capsule. Whereas the articular cartilage of the facet joint is aneural, the subchondral bone, synovium, synovial folds, and joint capsule are innervated extensively (https://pubmed.ncbi.nlm.nih.gov/22470845/).

👉 This joint can have meniscus-like structures that improve joint congruency. Facet joints work in pairs, along with the intervertebral disc (IVD), to constrain the motion of the vertebrae while aiding in the transmission of spinal loads (https://pubmed.ncbi.nlm.nih.gov/29494214/).

👉 The largely sagittal orientation of the lumbar facet joint, in combination with the high degree of mutual convexity and concavity of the opposing joint surfaces in this region, enables a greater range of motion in terms of flexion, as well as higher resistance to axial rotation (https://pubmed.ncbi.nlm.nih.gov/10529057/).

👉 In the lumbar spine, in vitro studies have shown that the facet articular surface alone bears 6–30% of axial compressive loads, depending on the mode of spinal motion (https://pubmed.ncbi.nlm.nih.gov/20881657/). The cervical and upper thoracic facet joints transmit 23% of axial compressive loads (https://pubmed.ncbi.nlm.nih.gov/3693090/).

👉 Note that loads in the cervical spine are smaller than those in the lumbar spine (cervical spine: flexion/extension: 17–27 N, lateral bending: 17–40 N, axial rotation: 26–30 N versus lumbar spine: flexion/extension: 46–109 N, lateral bending: 10–75 N, axial rotation: 56–120 N. (https://pubmed.ncbi.nlm.nih.gov/24661835/, https://pubmed.ncbi.nlm.nih.gov/24094992/, https://pubmed.ncbi.nlm.nih.gov/16198356/)

👉 Osteoarthritis (OA) of the facet joint is strongly associated with degeneration of the intervertebral disc (IVD) due to their intrinsically linked biomechanics. This relationship was originally described as a cascade of degenerative events initiated either by the facet joints or by the disc (https://pubmed.ncbi.nlm.nih.gov/6210480/). It is believed that facet degeneration usually follows disc degeneration, with facet overloading resulting from disc incompetence (https://pubmed.ncbi.nlm.nih.gov/2326704/, https://pubmed.ncbi.nlm.nih.gov/10552323/).

☝️ However, this sequence has been challenged by studies that have found facet joint OA in the absence of disc degeneration (https://pubmed.ncbi.nlm.nih.gov/21914197/, https://pubmed.ncbi.nlm.nih.gov/17767079/).

☝️ Ironically, surgical treatments of degenerated discs like spinal fusion or disc arthroplasty can encourage facet OA progression and induce adjacent segment disease (ASD, https://pubmed.ncbi.nlm.nih.gov/15534420/, https://pubmed.ncbi.nlm.nih.gov/25102498/, https://pubmed.ncbi.nlm.nih.gov/22706091/, https://pubmed.ncbi.nlm.nih.gov/21587111/).

👉 Degeneration of the facet joint might play a significant role in other back-related morbidities, such as degenerative spinal stenosis (progression of facet joint hypertrophy with subsequent development of osteophytes can compress spinal neural elements, leading to neurogenic intermittent claudication) degenerative spondylolisthesis (https://pubmed.ncbi.nlm.nih.gov/29494214/) and trauma (https://pubmed.ncbi.nlm.nih.gov/22020601/, https://pubmed.ncbi.nlm.nih.gov/28025352/).

📷Illustration: Pathophysiologic aspects of facet joint pain, https://link.springer.com/chapter/10.1007/978-1-4419-0352-5_10

11/10/2023

Low-grade inflammation 🔥 in intervertebral disc degeneration.

👉Degeneration of intervertebral disc (IVD) is weakly associated with long term pain and disability outcomes in patients with low back pain (LBP) (https://pubmed.ncbi.nlm.nih.gov/36914521)

👉It is increasingly recognized that, just like the cells of synovial membrane, resident disc cells and migrated immunocompetent cells possess the ability to mount a robust inflammatory response 🔥 against DAMPs and pathogen-associated molecular patterns (https://pubmed.ncbi.nlm.nih.gov/16508552/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2575634/).

👉 Damage-associated molecular patterns (DAMPs), also known as alarmins, and pathogen-associated molecular patterns are molecules released by stressed cells undergoing necrosis that act as endogenous danger signals to promote and exacerbate the inflammatory response 🔥.

👉 These biochemical features have been associated with patterns of structural damage including a condensed and fibrotic ECM, radial fissures, and indentations-herniations of nucleus pulposus into the vertebral endplate, annulus fibrosus rim lesions, delamination, and ingrowth of nerves and vessels in the disrupted otherwise aneural and avascular annulus fibrosus.

👉 Multiple factors including nonphysiological mechanical stresses, genetic predisposition, age-related changes, disc nutritional imbalance, environmental factors including smoking and vibration, as well as diabetes and infection all come into play to disrupt the already fragile and challenging homeostasis of IVDJ tissues (https://pubmed.ncbi.nlm.nih.gov/23015552/, https://pubmed.ncbi.nlm.nih.gov/26562470/ https://pubmed.ncbi.nlm.nih.gov/16915105/, https://pubmed.ncbi.nlm.nih.gov/24753325/, https://pubmed.ncbi.nlm.nih.gov/24436866/)

👉 Primary biochemical features of the degenerated discs include, but are not limited to ECM breakdown including fragmentation and reduced synthesis of proteoglycans, increased levels of inflammatory cytokines including TNF-α, IL-1B, matrix degrading, proteolytic enzymes of the MMP and ADAMTS families and collagen cross-linking in parallel with a synthesis of aberrant types of collagens (fibrosis), the presence of NGF and BDNF and a decrease of TGF-β, as well as a loss of cell density and water (https://pubmed.ncbi.nlm.nih.gov/16915105/, https://pubmed.ncbi.nlm.nih.gov/25827971/, https://pubmed.ncbi.nlm.nih.gov/10870137/, https://pubmed.ncbi.nlm.nih.gov/16508552/, https://pubmed.ncbi.nlm.nih.gov/9250186/).

👉 This structural damage eventually extends into the nucleus pulposus, and leads to an accelerated cell senescence and cell apoptosis (figure, https://pubmed.ncbi.nlm.nih.gov/24753325/, https://pubmed.ncbi.nlm.nih.gov/24436866/, https://pubmed.ncbi.nlm.nih.gov/10851095/, https://pubmed.ncbi.nlm.nih.gov/16816945/

📷 Figure: https://pubmed.ncbi.nlm.nih.gov/29355455/
DAMP: Damage-associated molecular pattern; ECM: Extracellular matrix; MMPs: Matrix-degrading enzymes metalloproteinases; TLRs: Toll-like receptors., ADAMTs: A Disintegrin and Metalloproteinase with Thrombospondin Motifs

16/07/2023

Witam

Aktualnie przebywam na urlopie i na wszystkie wiadomości i telefony postaram się odpowiedzieć do 21.07.2023
Jest dużo osób dzwoniących i piszących , dlatego proszę się przypominać 🙂

Z racji braków możliwości kontaktu telefonicznego i mojej kompletnej nieobecności - zawsze możecie pisać - postaram się na wszystko odpowiedzieć 🙂

Pozdrawiam 💪👍😊

19/06/2023

Dzień dobry

Istnieje codziennie mnóstwo pytań o wolny termin - udało wprowadzić się poprawki i w linku podanym niżej - jest możliwość wpisania się na listę rezerwowa 🙂

https://zarejestrowani.pl/w/7BdaQO8MyjQn4FecuzvuNw/

Będę indywidualnie informował Was o możliwościach i terminach jak i przesyła zainteresowanym taki link 🙂

Pozdrawiam i spokojnego , słoneczko dnia 😊💪

24/02/2023

Suspension Bridge of the Shoulder: the Rotator Cable ⛩

👉 The rotator cable (RC) is described as a thin fibrous band continuous with the coracohumeral ligament that courses along the undersurface of the rotator cuff fibers superficial to the joint capsule.
https://pubmed.ncbi.nlm.nih.gov/31207091/

👉 This fibrous band is located at the medial aspect of the relatively hypovascular crescentic region of the distal supraspinatus and infraspinatus tendons (rotator crescent), which is prone to injury
https://pubmed.ncbi.nlm.nih.gov/17057069/.

👉 The RC presents an anterior insertion on the superior facet of the lesser tubercle, an intermediate insertion on the anterosuperior edge of the greater tubercle and a posterior insertion to the inferior edge of the infraspinatus tendon.

👉 Cadaveric dissections have clearly demonstrated a tight connection between the rotator cuff tendons and the RC where the deep tendon fibers of the supraspinatus tendon reach the footprint on the greater tubercle of humerus through the RC and the capsule (i.e. shared fibers).
https://pubmed.ncbi.nlm.nih.gov/27139230/

👉 In this sense, the RC can be considered a pivotal anatomical structure through which the rotator cuff muscle-tendon units dynamize the glenohumeral capsule of the shoulder during active motions.
https://pubmed.ncbi.nlm.nih.gov/27916191/

👉 Of note, the glenohumeral capsule presents a wide attachment area occupying from 30% to 61% of the greater tuberosity footprint on the humerus (https://pubmed.ncbi.nlm.nih.gov/21816631/). This anatomical detail is strongly related with the important role of the superior capsule in providing superior glenohumeral stability (https://pubmed.ncbi.nlm.nih.gov/27916191/).

💡 Based on the current available anatomical findings; the rotator cuff tendons, the RC and the glenohumeral capsule should not be considered different structures but rather a unique functional unit of the shoulder (https://pubmed.ncbi.nlm.nih.gov/31207091/).

⛩ The cable-crescent complex is mentioned to resemble a ‘suspension bridge’ (s. figure in comments), where the biomechanical load is transmitted to the cable which distributes the stress to the humerus (https://pubmed.ncbi.nlm.nih.gov/8305096/). As long as the cable and its insertions are intact, the rotator cuff fibers can maintain shoulder strength and range of motion even in the presence of full-thickness tears of the crescent fibers. If the cable becomes compromised, then the cuff will lose its main stabilizing structure, leading to progressive, worsening shoulder symptoms (https://pubmed.ncbi.nlm.nih.gov/30931149/).

Even in cases of partial thickness rotator cuff tears involving the RC, there are significant changes in joint translation (https://pubmed.ncbi.nlm.nih.gov/24132354/). Moreover, the portion of RC localized under the most anterior section of the supraspinatus tendon immediately posterior to the bicipital groove (portion attaching to the anterosuperior edge of the greater tubercle) seems to be the most important in transmitting mechanical forces from the rotator cuff to the proximal part of the humerus (https://pubmed.ncbi.nlm.nih.gov/24132354/).

Illustration: Iriarte, I., Pedret, C., Balius Matas, R., & Cerezal, L. (2021). Ultrasound of the musculoskeletal system: Anatomical exploration and pathology. MSK Books.