Ortho Kinos

29/08/2025

04/08/2025

11/06/2025

05/02/2025

L’Entrapement du Nerf de Baxter

🦶 La douleur plantaire du talon est l’une des affections podiatriques les plus courantes et les plus persistantes. Des études estiment que 10 à 15 % de la population en souffrira au cours de sa vie (source, source). Cependant, poser un diagnostic précis est difficile en raison des nombreuses causes possibles, telles que la fasciopathie plantaire, l’atrophie du coussinet adipeux et l’entrapement nerveux, qui présentent des symptômes similaires (source, source).

🦶 Parmi ces causes, l’entrapement de la première branche du nerf plantaire latéral, également appelée nerf de Baxter (BN) ou nerf calcanéen inférieur, est considéré comme l’une des principales sources de neuropathie, représentant environ 20 % des cas de douleur chronique du talon (source).

🦶 Décrit pour la première fois en 1984 par Baxter et Thigpen, il est souvent sous-estimé comme cause de douleur médiale du talon, notamment chez les sportifs, où il peut coexister avec une fasciopathie plantaire (source).

🦶 Généralement issu du nerf plantaire latéral (NPL) juste après son origine à partir du nerf tibial, le BN est un nerf mixte, à la fois moteur et sensitif. Il contient une branche motrice pour le muscle abducteur du petit orteil (ADM) et une branche sensitive (appelée branche calcanéenne du nerf calcanéen inférieur) qui innerve le périoste du tubercule médial du calcanéum ainsi que le ligament plantaire long (source).

👉 Deux sites principaux d’entrapement du BN sont bien connus (source) :

1️⃣ Premier site : Lorsque le nerf traverse le fascia profond de l’abducteur de l’hallux, entre ce muscle et la bordure caudale médiale du muscle carré plantaire (source). Les facteurs contributifs incluent des anomalies biomécaniques comme un pied creux ou une pronation excessive, ainsi qu’une hypertrophie musculaire.

2️⃣ Deuxième site : Là où le nerf passe juste en avant du tubercule médial du calcanéum. Les facteurs contributifs incluent une fasciopathie plantaire ou une épine calcanéenne (source, source).

👉 Cliniquement, les patients souffrant d’un entrapement du nerf de Baxter présentent une douleur plantaire du talon, mais avec des différences subtiles par rapport à ceux atteints de fasciopathie plantaire.

✅ Les patients décrivent une douleur située plus médialement que celle observée dans la fasciopathie plantaire.

✅ De plus, la douleur est souvent décrite comme une sensation de brûlure sur le côté médial du talon, aggravée en soirée et après l’activité physique, contrairement à la douleur matinale caractéristique de la fasciopathie plantaire (source, source).

✅ Un signe de Tinel positif et une sensibilité maximale aux sites d'entrapement permettent de confirmer le diagnostic (source). Les patients peuvent également signaler un engourdissement ou des paresthésies sur la partie latérale du pied, surtout dans les cas chroniques (source).

✅ L’examen de ces entrapements nerveux doit inclure une évaluation biomécanique afin de détecter d’éventuelles anomalies, comme un varus ou un valgus du pied, un équin ou un pied plat.

💡 La prise en charge initiale de la neuropathie de Baxter repose sur une combinaison de gestion de la charge, d’anti-inflammatoires non stéroïdiens (AINS), d’orthèses et de physiothérapie (renforcement des muscles intrinsèques du pied, mobilisation neurale, source, source, source). Cependant, ces approches reposent sur des preuves scientifiques limitées (source).

📸 Source : Dissection anatomique du nerf de Baxter, qui diverge du nerf plantaire latéral. Il suit une trajectoire verticale avant de se courber horizontalement (flèche rouge) vers le muscle abducteur du petit orteil. BN : nerf de Baxter, NPL : nerf plantaire latéral, NPM : nerf plantaire médial, FHL : muscle long fléchisseur de l’hallux, FDL : muscle long fléchisseur des orteils.

20/01/2025

Cette étude de Hoch et ses collègues apporte des éclairages précieux sur les rôles du tensor fasciae latae (TFL), du gluteus medius/minimus (Gmed/min) et du gluteus maximus (Gmax) dans l'abduction de la hanche. Voici une synthèse des principaux résultats et de leurs implications :

Principaux résultats
Tensor Fasciae Latae (TFL) :

Le TFL joue un rôle mineur dans l'abduction de la hanche, contribuant principalement lors d'une flexion de hanche à 30° (réduction de 15 % de la force après paralysie).

Sa contribution dans les positions neutres et en extension de la hanche était négligeable.

Cela confirme les fonctions principales du TFL : la flexion de la hanche et la stabilisation du genou via la bande iliotibiale.

Gluteus Medius et Minimus (Gmed/min) :

Ces muscles sont les principaux contributeurs à l'abduction de la hanche, représentant plus de 60 % de la force d'abduction dans toutes les positions de la hanche.

La paralysie de ces muscles a entraîné une réduction des deux tiers de la force d'abduction, rendant certaines tâches impossibles pour certains participants.

Cela souligne leur rôle crucial dans la stabilité de la hanche et la locomotion.

Gluteus Maximus (Gmax) :

Le Gmax s'est révélé être un contributeur significatif à l'abduction de la hanche, en particulier dans les positions fléchies, avec une réduction de force de 43 à 56 % après paralysie.

Cela remet en question la vision traditionnelle du Gmax comme principalement extenseur et rotateur externe de la hanche, mettant en lumière son rôle potentiel dans la compensation d'une faiblesse des abducteurs.

Implications cliniques
Rééducation et préhabilitation :

Renforcer le Gmax pourrait être une stratégie utile pour compenser une insuffisance des abducteurs de la hanche, notamment chez les patients atteints de troubles neurologiques ou se préparant à une chirurgie de la hanche.

Bien que le rôle du TFL dans l'abduction soit limité, sa contribution lors de la flexion de la hanche suggère qu'il pourrait jouer un rôle dans des protocoles de rééducation spécifiques.

Stabilité et fonction de la hanche :

La dominance des Gmed/min dans l'abduction renforce l'importance de cibler ces muscles dans les programmes visant à améliorer la stabilité de la hanche et la mécanique de la marche.

L'implication du Gmax dans l'abduction, en particulier lors de la flexion, suggère qu'il pourrait aider à maintenir la fonction lors d'activités comme monter des escaliers ou se lever d'une position assise.

Limites de l'étude
Mesures statiques :

L'étude a mesuré l'abduction dans des positions statiques, ce qui ne reflète pas nécessairement les mouvements dynamiques de la vie réelle.

Faiblesse aiguë vs chronique :

L'utilisation de blocs nerveux aigus ne tient pas compte des mécanismes compensatoires qui se développent en cas de faiblesse musculaire chronique.

Différenciation musculaire :

L'étude n'a pas différencié les parties antérieure, moyenne et postérieure des Gmed/min ou du Gmax, qui pourraient avoir des rôles fonctionnels distincts.

Conclusion
Cette étude met en lumière l'interaction complexe entre le TFL, les Gmed/min et le Gmax dans l'abduction de la hanche. Bien que les Gmed/min restent les principaux abducteurs, le Gmax joue un rôle sous-estimé jusqu'ici, en particulier dans les positions fléchies. Ces résultats pourraient orienter des stratégies de rééducation ciblées pour les patients présentant une insuffisance des abducteurs de la hanche, en insistant sur l'importance de renforcer à la fois les Gmed/min et le Gmax.

11/12/2024

Just published in NEJM 🔥

Degenerative Rotator-Cuff Disorders

📘 https://www.nejm.org/doi/full/10.1056/NEJMcp1909797

👉 Rotator-cuff disorder encompasses a spectrum of tendon degeneration, including (in order of increasing severity) rotator-cuff tendinopathy, partial-thickness tears, full-thickness tears, and rotator-cuff–tear arthropathy (a chronic rotator-cuff tear that leads to superior migration of the humeral head and arthritis over time). (https://pubmed.ncbi.nlm.nih.gov/39602631/, https://pubmed.ncbi.nlm.nih.gov/38332156/)

👉The rotator cuff comprises four tendons: supraspinatus (assists with abduction of the arm), infraspinatus (assists with external rotation of the arm), subscapularis (assists with internal rotation), and teres minor (assists with external rotation. (figure from https://pubmed.ncbi.nlm.nih.gov/39602631/)

👫 The incidence of surgery for rotator-cuff disorder, the most common cause of shoulder pain, across U.S. states ranges from 12 to 185 per 100,000 (https://pubmed.ncbi.nlm.nih.gov/31825507/).

🤕 Tears of the rotator cuff can result from substantial traumatic injury (e.g., a motor vehicle accident, assault, a blow from a fast-moving projectile, or a fall from greater than standing height, https://pubmed.ncbi.nlm.nih.gov/31397866/) or can occur insidiously (atraumatic or degenerative rotator-cuff tear).

👴 Age above 40 years is by far the strongest risk factor for degenerative tears (https://pubmed.ncbi.nlm.nih.gov/30335631/), with increasing prevalence with advancing age (https://pubmed.ncbi.nlm.nih.gov/25441568/): 1/5 in the 50s and 1/3 in the 80s. It is interesting to know that the prevalence of asymptomatic tear also increased with age: 1/2 in the 50s and 2/3 in those older than 60s, (https://pmc.ncbi.nlm.nih.gov/articles/PMC3768248/).

🫀Several disease conditions have been postulated to have a role in the development and progression of rotator cuff disease, and subsequently, may influence healing rates following surgical repair. These conditions include type 2 diabetes mellitus, hyperlipidaemia, s*x hormone deficiency, obesity, smoking, hypertension, gout, connective tissue diseases and depression (https://pubmed.ncbi.nlm.nih.gov/34660827/, https://pubmed.ncbi.nlm.nih.gov/34424222/, https://pubmed.ncbi.nlm.nih.gov/30808669/, https://pubmed.ncbi.nlm.nih.gov/27600100/, https://pubmed.ncbi.nlm.nih.gov/28486089/, https://pubmed.ncbi.nlm.nih.gov/36252786/)

🫀 In natural-history studies of degenerative rotator-cuff tears, at 5 years of follow-up, the tears were enlarged in half the persons with full-thickness tears (https://pubmed.ncbi.nlm.nih.gov/31627964/) and the tears had progressed to full thickness in approximately one third of those with partial-thickness tears (https://pubmed.ncbi.nlm.nih.gov/26589385/). But there is a lack of correlation between patient symptoms and the size and thickness of the tear on imaging (https://pubmed.ncbi.nlm.nih.gov/24875019/).

📶Full-thickness tears are classified according to Codman classification (https://pubmed.ncbi.nlm.nih.gov/34012769/, tear size in anterior to posterior direction) as:

• Small: 0–1 cm
• Medium: 1–3 cm
• Large: 3–5 cm
• Massive: >5 cm

Although there is expert consensus that traumatic rotator-cuff tears should be treated operatively timely soon after the diagnosis is made to avoid long-term consequences such as rotator-cuff muscle degradation and tendon retraction (https://pubmed.ncbi.nlm.nih.gov/24292934/), most patients with symptomatic degenerative rotator cuff disorders can be treated nonoperatively.

🏋️‍♂️ Nonoperative treatment using an exercise based protocol is effective for treating atraumatic full-thickness rotator cuff tears in approximately 75% of patients followed up for 2 years (https://pubmed.ncbi.nlm.nih.gov/23540577/), 5 years (https://www.jshoulderelbow.org/article/S1058-2746(18)30852-8/abstract) and even 10 years (https://www.sciencedirect.com/science/article/pii/S2666638324004778). Compared with natural history, patients who performed physical therapy within the first 3 months had statistically significant improvements in pain and function as measured by the SPADI score at 3 months (https://pubmed.ncbi.nlm.nih.gov/30553798/).

😷 Consensus is lacking regarding indications for surgical intervention. Observational data support that surgery is associated with better function and reduced pain in patients who are younger (e.g.,

07/12/2024

Spectrum of Rotator Cuff Disease 💡

▶️ Rotator cuff (RC) tears represent a spectrum of disease, from tendinopathy, to partial-thickness tears and to full-thickness tears of varying sizes (s. figure, modified after Bedi et al. 2024, https://pubmed.ncbi.nlm.nih.gov/38332156/)

⬛ RC tendinopathy

▶️ The proposed mechanisms of RC tendinopathy include intrinsic, extrinsic, or combined mechanisms (https://pubmed.ncbi.nlm.nih.gov/18801774/, https://pubmed.ncbi.nlm.nih.gov/20846766/, https://pubmed.ncbi.nlm.nih.gov/26390274/)

1️⃣ External mechanisms are characterized by inflammation of the bursa above the rotator cuff and bursal-sided RC tendon compression due to altered shoulder kinematics. When the larger muscles (deltoid) over-compensate due to rotator cuff dysfunction, the rotator cuff cannot function as an effective force couple, resulting in the humeral head elevating rather than depressing during shoulder motion (https://pubmed.ncbi.nlm.nih.gov/6825348/). This abnormal motion exacerbates bursal inflammation, causing pain during motion, overhead activities, and sleep (https://pubmed.ncbi.nlm.nih.gov/38332156/). But for years, the theory of external shoulder impingement has been strongly questioned scientifically (https://www.tandfonline.com/doi/abs/10.1179/1743288X11Y.0000000027, https://pubmed.ncbi.nlm.nih.gov/33244115/, https://pubmed.ncbi.nlm.nih.gov/30707445/).

A unique subset of RC tendinopathy with an extrinsic mechanism is internal impingement. Patients with internal impingement tend to present with pain located in the posterior and superior aspects of the shoulder typically while the arm is in abduction and external rotation of the late cocking phase of throwing (https://pubmed.ncbi.nlm.nih.gov/8534293/, https://pubmed.ncbi.nlm.nih.gov/8504590/). In this position, the articular aspect of the RC tendons becomes mechanically impinged between the posterior superior glenoid rim and the humeral head (https://pubmed.ncbi.nlm.nih.gov/20846766/).

2️⃣ There is a growing body of evidence to support an intrinsic mechanism. Intrinsic mechanisms relate to factors that directly influence tendon health and quality, including aging, (https://pubmed.ncbi.nlm.nih.gov/10471998/) genetics, (https://pubmed.ncbi.nlm.nih.gov/19411462/) vascular changes, (https://pubmed.ncbi.nlm.nih.gov/19293165/) and altered loading (https://pubmed.ncbi.nlm.nih.gov/19364757/).

▶️ Tendinopathy as a potential precursor to tears, exhibits disorganized collagen, increased inflammatory cells, and reduced vascularity. However, symptoms do not consistently correlate with the histopathological severity of tendinopathy or the extent of rotator cuff tears. The prevalence of asymptomatic partial-thickness and full-thickness RCTs has been reported to range from 8% to 40% and from 0% to 46%, respectively (https://pmc.ncbi.nlm.nih.gov/articles/PMC7026731/). This disconnect underscores the complex interplay between structural degeneration, inflammation, and pain perception, which may be influenced by central nervous system mechanisms (https://pubmed.ncbi.nlm.nih.gov/38332156/).

⬛ Progression of the disease

The progression from tendinopathy to partial- and full-thickness tears is not fully understood but is thought to begin with a failed healing response to microtrauma and the role of inflammation in these conditions has been re-evaluated and is thought to be an important contributor (https://pubmed.ncbi.nlm.nih.gov/15634833/, https://pubmed.ncbi.nlm.nih.gov/28596062/). This involves increased inflammation mediated by tenocytes and immune cells releasing pro-inflammatory cytokines such as TNF, IL-6, and IL-1β. IL-17A, in particular, is notable for its role in promoting inflammation and apoptosis in rotator cuff tendons (https://pubmed.ncbi.nlm.nih.gov/27263531/).

⬛ Pain and the neuroimmune system
An upregulation of the glutamatergic system has been observed in patients with rotator cuff tendinopathy. Glutamate localizes to tenocytes and is detected on macrophage glutamate receptors, suggesting its role in pain modulation (https://pubmed.ncbi.nlm.nih.gov/24872365/).

▶️ In summary, rotator cuff disease evolves from biomechanical dysfunction and inflammatory responses to chronic structural degeneration, with pain perception influenced by neuroimmune changes. The bursa and inflammatory pathways, particularly IL-17A, represent key areas for understanding disease mechanisms and potential therapeutic interventions.

▶️ A review by Lo and colleagues in 2023 found biochemical changes such as inflammatory molecules in the subacromial bursa, levels of IL‐1 β and IL‐6 in the synovial fluid of the glenohumeral joint and serum levels of VEGF to demonstrate moderate to strong correlations (r = 0.66–0.75) with rotator cuff related shoulder pain.

📸 Figure modified after Bedi et al. (https://pubmed.ncbi.nlm.nih.gov/38332156): Representative pathology and functional differences in rotator cuff pathology. RC-tendinopathy, partial-thickness and small full-thickness tears present with similar symptoms, with pain on overhead activity, pain at night and variable findings on clinical examination. Patients with larger and massive tears will have lost their force couple and have difficulty elevating their arm, and are more likely to have a positive external rotation lag test than patients with small tears.

01/12/2024

Just published 🔥

Adipose Tissue Around the Knee; a Pictorial Review of Normal Anatomy and Common Pathologies

📘 https://www.sciencedirect.com/science/article/pii/S0363018824002123

🦵 The fat pads around the knee compromise IAFPs and Periarticular fat pads. IAFPs consist of Infra-patellar Fat Pad (IPFP), known as Hoffa fat pad, Suprapatellar Fat Pad (SPFP), Pericruciate Fat Pad (PCFP), and prefemoral Fat Pad (PFFP) (s. figure below, https://pubmed.ncbi.nlm.nih.gov/27118690/). The main component of periarticular adipose tissue is subcutaneous fat, located on the anterior aspect of the knee, just below the skin (https://pubmed.ncbi.nlm.nih.gov/22664860/).

🦵 Intra articular fat pads (IAFPs) are intra-capsular, extra-synovial structures that are particularly important in shock absorption and mechanical support of cartilage, menisci, and ligaments https://pubmed.ncbi.nlm.nih.gov/28993563/98 In other words, intra-articular fat pads adapt their morphology dynamically following the knee movement and accommodate the joint spaces to reduce friction between intra-articular structures (s. figure).

👉 So, these fat pads serve as dynamic and adaptable structures. They help accommodate joint motion, reduce friction, and absorb mechanical stress. Additionally, their vascular and neural components contribute to joint health, nociception, and inflammatory responses.

🔑 The key fat pads include:

1️⃣ Infrapatellar Fat Pad (Hoffa's Fat Pad; in Red)

▶︎ IPFP is the largest intra-articular adipose tissue of the knee. It is an intra-articular, intra-capsular, and extra synovial structure with internal fibrous scaffold filled with fat tissue. This trapezoidal fat pad occupies the space between the inferior pole of patella, patellar tendon, proximal tibia, and the distal femoral condyles. It is bounded by the inferior pole of the patella and patellar tendon anteriorly and the anterior horns of both menisci posteriorly (https://pubmed.ncbi.nlm.nih.gov/15678298/).

👉Functions:

▶︎ Acts as a shock absorber.

▶︎ Facilitates smooth movement by reducing friction between the patellar tendon, tibia, and femur.

▶︎Provides neurovascular support to the knee joint.


2️⃣ Suprapatellar Fat Pad (in Green)

▶︎ Suprapatellar fat pad (SPFP), also known as the quadriceps fat pad, is a triangular shaped structure in the sagittal plane. Its anterior border lies just posterior to quadriceps tendon, and the inferior border attaches to the upper part of patella. SPFP is located anterior to the suprapatellar recess and is covered with synovium posteriorly.

👉 Functions:

▶︎ Protects the suprapatellar bursa and reduces friction during knee extension and flexion.

▶︎ Accommodates knee movement by deforming to reduce intra-articular pressure.

3️⃣ Prefemoral Fat Pad (in Blue):

▶︎ Prefemoral fat pad (PFFP), the smallest and the least investigated fat pad, is located anterior to the distal femoral metaphysis above the femoral trochlea. It is covered by synovium anteriorly (https://pubmed.ncbi.nlm.nih.gov/22664860/).

👉 Functions:

▶︎ Offers cushioning and prevents impingement of soft tissues during movement.

4️⃣ Pericruciate Fat Pad (in Yellow):

▶︎ Pericruciate fat pad (PCFP) is a triangular shaped intracapsular extra-synovial structure located in the posterior aspect of the knee.

▶︎ PCFP is superior and between the cruciate ligaments, near their attachment sites within the intercondylar fossa of the femoral condyles. It is superomedial to the posteromedial bundle of the ACL.

▶︎ PCFD has close contact with the posterior capsule. It is covered by synovium, which is thicker both anteriorly and posteriorly (https://www.sciencedirect.com/science/article/pii/S2214854X21000327).

👉 Functions:

▶︎ Reduces friction between the cruciate ligaments and surrounding structures.
▶︎ May assist in stabilizing the ligaments during motion.

👉 Fat pads are prone to pathological changes, such as edema, impingement, or mass-like lesions, which can be evaluated effectively through imaging modalities like MRI..

24/11/2024

Just published 🔥

Tendon Cell Biology: Effect of Mechanical Loading 🦶

👉 Tendons are primarily composed of longitudinal bundles of collagen fibers that connect muscle to bone (https://pubmed.ncbi.nlm.nih.gov/10418074/). The backbone of the tendon is formed by Type I collagen, which is crucial for force transmission (https://pubmed.ncbi.nlm.nih.gov/28882761/). Other components of the tendon extracellular matrix include various collagen isoforms, glycoproteins, proteoglycans, and water (https://pubmed.ncbi.nlm.nih.gov/39568406/). Collagen accounts for approximately 70-80% of the adult tendon’s dry weight (https://pubmed.ncbi.nlm.nih.gov/17205554/), with Type I collagen constituting 65-80% of this total collagen content (https://pubmed.ncbi.nlm.nih.gov/24818782/). Water makes up about 55-70% of the wet mass of the tendon (https://pubmed.ncbi.nlm.nih.gov/14340913/).

👉 Tendons possess a remarkable ability to adapt to various types of mechanical loads, with the most notable adaptations occurring in response to tensile and compressive forces. There are three primary types of mechanical loads experienced by tendons within the musculoskeletal system: tension (where the tissue is pulled in one direction), compression (where the tissue is pushed from one or more directions), and shear (where the tissue is subjected to sliding forces). These adaptive processes begin as early as in utero (https://pubmed.ncbi.nlm.nih.gov/24316363/).

📘 In a brand-new paper, Stańczak et al. explore the mechanisms of mechanotransduction and tendon adaptations to mechanical loading (https://pubmed.ncbi.nlm.nih.gov/39568406/

👉 Mechanotransduction is a critical process that enables tendon cells, such as tenocytes and tendon stem/progenitor cells, to sense and respond to mechanical stimuli, converting external forces into intracellular biochemical signals that regulate cell behavior, matrix remodeling, and tissue homeostasis (s. figure, https://pubmed.ncbi.nlm.nih.gov/25355505/). This process is fundamental for maintaining tendon health, as it allows cells to adapt to varying mechanical environments, ensuring that tendons can withstand repetitive loading and respond effectively to changes in mechanical demand (https://pubmed.ncbi.nlm.nih.gov/25640030/).

👉 Mechanotransduction is initiated at the cell membrane, where mechanosensitive receptors like integrins form complexes with focal adhesion proteins, including vinculin, talin, and paxillin. These complexes physically link the ECM to the actin cytoskeleton, transmitting mechanical signals into the cell (https://pmc.ncbi.nlm.nih.gov/articles/PMC149854/. This signal transmission activates intracellular pathways such as MAPK/ERK, Rho/ROCK, and PI3K/Akt, which are critical for regulating gene expression, cytoskeletal organization, and protein synthesis (https://pubmed.ncbi.nlm.nih.gov/16000201/).

The figure below illustrates the process of mechanotransduction in tendons in response to mechanical loading, highlighting the molecular pathways that regulate tendon adaptation:

1️⃣ Upon the application of mechanical loading, such as ground reaction forces during running or high intensity strength training, the extracellular matrix (ECM) experiences stress propagation from the macro to the micro-level, activating mechanosensitive receptors on tenocytes [mechanical loading phase].

2️⃣ This mechanical signal is then converted into biochemical signals within the tendon cells through ECM-cell interactions, involving integrins, focal adhesion complexes, and cytoskeletal elements, initiating intracellular pathways like MAPK/ERK and Rho/ROCK [signal conversion].

3️⃣ As a result, tenocytes increase the synthesis of new matrix components such as collagen and proteoglycans, promoting the remodeling of the ECM and degradation of damaged matrix [matrix synthesis and degradation].

4️⃣ This remodeling process leads to the incorporation of newly synthesized molecules into the ECM, enhancing its structural and functional integrity [ECM incorporation]. This elevated collagen expression is probably regulated by the strain imparted on the fibroblast, which can induce a 2–3-fold increase in collagen formation that peaks around 24 h after loading and remains elevated for up to 70–80 h. The degradation of collagen proteins also increases in response to exercise, probably early on and to a greater extent than collagen synthesis (https://pubmed.ncbi.nlm.nih.gov/16002437/, https://pubmed.ncbi.nlm.nih.gov/10066916/)

5️⃣ The final result is a sustained or improved tendon function, ensuring that the tissue can better withstand subsequent mechanical loads [functional adaptation]. Ultimately, the cycle contributes to tissue homeostasis and adaptation, preventing overuse injuries and maintaining tendon health.

☝️ But…. after cessation of physical loading and up to 18–36 h thereafter (improved training status shortens this time frame) there is a negative net balance in collagen levels, whereas the balance is positive (anabolic in relation to collagen) for up to 72 h after loading). These data indicate that a net increase in collagen requires a certain restitution period, and that without sufficient rest a continuous loss of collagen is likely to occur, which might render the tendon vulnerable to injury (https://pubmed.ncbi.nlm.nih.gov/20308995/). The prescription of twice daily (i.e. the original Alfredson protocol) or daily tendon loading programs, might therefore be suboptimal from a tendon biology perspective (https://bjsm.bmj.com/content/57/20/1327).

💡 Clinical Implications: Understanding tendon biology and mechanotransduction can inform therapeutic strategies, such as load-based rehabilitation and targeting specific molecular pathways to enhance tendon repair and prevent degenerative conditions.