A Mechanical Hypothesis of Deep Sclerotic Fibrous Tissue in the Dorsocervical Hump as the Dominant Passive Constraint in Forward Head Posture: Multi-Pathway Origins and Testable Predictions

1. Introduction

Forward head posture (FHP) refers to a postural pattern in which the center of gravity of the head is displaced anteriorly relative to the trunk in the sagittal plane; clinically, it is often quantified by the craniovertebral angle, with a smaller craniovertebral angle indicating more severe forward posture. The widespread use of handheld electronic devices has made this posture increasingly common among young people. The existing FHP literature is predominantly focused on rehabilitation and exercise therapy: therapeutic exercise can improve the craniovertebral angle and neck function, but effect sizes are limited and the certainty of evidence is mostly low to moderate. A systematic review and meta-analysis of 10 randomized controlled trials (RCTs) involving 550 patients with FHP and neck pain reported that therapeutic exercise improved the craniovertebral angle compared with control, with a pooled effect size of mean difference (MD) = 3.38° (95% confidence interval [CI] 2.10–4.65), standardized mean difference (SMD) = 0.95 (95% CI 0.61–1.28), and low to moderate certainty of evidence (1). This pooled estimate provides a quantitative benchmark against which Prediction 4 below can be compared. Biomechanical studies have shown that FHP is associated with alterations in balance, proprioception, and respiratory function. These studies have addressed what accompanies FHP and how to train, but have rarely addressed a more fundamental mechanical question head-on: in individuals with long-standing FHP, what physically locks the forward posture in place?

In the existing explanatory framework, the maintenance of FHP is attributed to muscle imbalance (weakness of the deep cervical flexors and tightness of the superficial extensors) and behavioral habits (screen use and head-down posture). The deep sclerotic fibrous tissue of the dorsocervical hump—subcutaneous fat pad at the cervicothoracic junction accompanied by deep investing fascial fibrosis and sclerosis—is usually placed in one of two positions: it is described either as a secondary consequence of FHP or as a co-localized accompanying phenomenon. In this narrative, fibrosis and sclerosis are results, and their mechanical weight is regarded as secondary, lower than that of muscle and behavioral factors. A particular distinction must be made: the external volume of the dorsocervical hump is mainly contributed by the superficial fat pad, whereas the hypothesis in this article targets the deep sclerotic fibrous tissue (anatomical definition in Section 2), not the volume or thickness of the fat pad. This distinction is not merely a logical inference: a cadaveric anatomical and histological study of the dorsocervical fat pad showed that the dorsocervical fat pad consists of superficial and deep adipose layers (2); another histological study comparing dorsocervical with abdominal subcutaneous adipose tissue showed that dorsocervical adipose tissue is surrounded by more prominent fibrous connective tissue, with a richer collagenous stroma surrounding adipocytes (3). Together, these findings provide direct human anatomical and supportive histological evidence that the superficial fat pad and deep tissue are distinct components at different anatomical layers and that fibrous connective tissue is more prominent in the dorsocervical region. Furthermore, a pathological study of surgical specimens from 86 patients with dorsocervical fibrofatty prominence used Masson staining to quantify collagen content and K-means clustering to identify three subtypes: a fat-dominant subtype (collagen content <23.3%), a mixed subtype (23.3–38.4%), and a fibrosis-dominant subtype (>38.4%) (4). This indicates that within the dorsocervical hump patient population, there does exist a subtype dominated by fibrous collagen and distinct from simple fat accumulation—sclerosis is not merely a theoretical construct but an entity that can be independently identified pathologically in patient specimens.

This narrative leaves a question that has not been systematically examined: in individuals with long-standing FHP, might the deep sclerotic fibrous tissue of the dorsocervical hump have already evolved from a secondary consequence into a dominant passive constraint, with a mechanical weight exceeding that of muscle and behavioral factors? The importance of this question lies in the following: if sclerotic tissue is merely an accompanying phenomenon, the focus of FHP intervention should be placed on muscle retraining and behavioral correction; if sclerotic tissue has become a dominant maintaining factor, then posture correction alone may encounter a passive mechanical resistance, and the logic of intervention would need to be adjusted accordingly.

This article proposes a falsifiable mechanical hypothesis and provides literature-based support, testable predictions, and validation pathways. We state at the outset that this article is a purely theoretical argument based on published literature and mechanical principles and contains no patient data or observational information from clinical practice; the value of the hypothesis lies in advancing a proposition worthy of rigorous testing, not in claiming that the proposition has been proven. This article focuses on the mechanistic level and does not discuss specific surgical methods or technical procedures.

2. Hypothesis

Core hypothesis: In individuals with long-standing forward head posture, the deep sclerotic fibrous tissue of the dorsocervical hump—that is, tissue at the cervicothoracic junction in which the investing fascia has undergone fibrosis and increased stiffness—may have evolved from a secondary consequence of FHP into a dominant passive constraint and may constitute the main mechanical resistance to returning the head to a neutral position. When sufficiently stiff, this tissue can generate a passive flexion moment as the cervical spine attempts to return to a neutral position. According to the operational threshold used in this article (see Section 3.8), dominance must be tested simultaneously by a mechanical threshold criterion and a joint model criterion: the mechanical threshold is a necessary but not sufficient condition, and only the joint model criterion directly compares the relative explanatory power of passive constraint, muscle function, and behavioral factors. The hypothesis targets sclerosis (increased stiffness), not increased volume or fat accumulation.

Anatomical definition. The operational anatomical localization of the deep sclerotic fibrous tissue of the dorsocervical hump as referred to in this article is as follows. From superficial to deep, the posterior cervical region consists of the skin, subcutaneous adipose tissue (including superficial and deep adipose layers (2)), the superficial layer of the deep cervical fascia (investing fascia, which envelops the trapezius and continues posteriorly with the nuchal ligament), the trapezius, the deep layer of the deep cervical fascia (prevertebral fascia), and the cervical osseous structures and nuchal ligament. The external volume of the dorsocervical hump is mainly contributed by the subcutaneous fat pad; the target deep sclerotic fibrous tissue in this article refers to fibrotic thickening and increased stiffness of the investing fascia posterior to the cervicothoracic junction (approximately at the C7–T1 level), and its anatomical scope includes the trapezius fascia itself, fibrous septa extending vertically from the investing fascia into the deep layer and anchoring to the deep cervical fascia and nuchal ligament, and fibrous tissue near the C6/C7 attachment of the nuchal ligament. These three components are anatomically continuous at the cervicothoracic junction and can be regarded mechanically as a coupled passive tension band system.

Several caveats apply to the evidence base for this definition: that the investing fascia envelops the trapezius and is continuous with the nuchal ligament is a standard anatomical description; that fibrous septa anchor to deep structures is supported by anatomical and imaging descriptions; that the dorsocervical fat pad has superficial and deep layers is supported by cadaveric anatomical and histological evidence (2); and that dorsocervical fibrous connective tissue is more prominent than in the abdomen is supported by comparative histological evidence (3). However, no independent anatomical study of the investing fascia at the C7–T1 level in patients with dorsocervical hump is currently available; the above definition is an operational construct assembled from standard anatomical descriptions, imaging descriptions, and histological evidence from adjacent regions, rather than a dedicated anatomical conclusion regarding the investing fascia in this region. The term “investing fascial fibrosis” as used in this article does not presuppose involvement of all three components described above or equal degrees of fibrosis among them; it is an operational designation for a mechanical functional unit, and the relative contribution of each component must be separated in future imaging–histological correlation studies. To avoid referential drift, this article specifies that deep sclerotic tissue in the core proposition requires only that the overall passive stiffness of this functional unit be increased; it does not require equal degrees of fibrosis across the investing fascia, fibrous septa, and nuchal ligament attachment sites. The relative contribution of each component is a validation question, not a prerequisite for the hypothesis to hold. For conciseness, deep sclerotic fibrous tissue of the dorsocervical hump is abbreviated hereafter as deep sclerotic tissue; the term sclerotic band is used only in mechanical reasoning to denote its functional role as a passive tension band.

Measurement definition of sclerosis: In this article, sclerosis refers to a tissue shear modulus measured by SWE that is significantly higher than that of normal posterior cervical tissue in age-matched individuals, or to a palpably hardened texture; its pathological basis is increased collagen deposition and cross-linking rather than simple fat thickening. Cadaveric anatomical and histological studies of the dorsocervical fat pad have confirmed that it consists of superficial and deep adipose layers (2), and dorsocervical subcutaneous adipose tissue contains more prominent fibrous connective tissue than abdominal subcutaneous adipose tissue (3), making sclerosis an anatomically and histologically measurable target independent of fat volume. Pathological classification of surgical specimens from dorsocervical hump further indicates that a fibrosis-dominant subtype with collagen content >38.4% exists objectively in the patient population (4), providing patient-level direct evidence for sclerosis as a pathological entity independent of fat volume. The same study reported that the accuracy of SWE in distinguishing fibrotic subtypes in this cohort was only 48.0%–67.2%, lower than the 92%–93% of B-mode ultrasound (4); therefore, SWE as a measurement tool for sclerosis in the dorsocervical hump region may be subject to interference from tissue heterogeneity, and B-mode ultrasound fibrosis scoring can serve as an auxiliary screening tool for subtype stratification, with the two being complementary rather than interchangeable.

Fascial pathology further distinguishes two changes that can both manifest as increased stiffness: densification and fibrosis. The former arises from altered viscosity of loose connective tissue and is reversible; the latter arises from structural alteration of fibrous layers and is irreversible (5). Sclerosis as used in this article does not presuppose reversibility, but this distinction suggests that stiffness elevation measured by SWE may reflect a mixture of both components. If stiffness mainly reflects reversible densification, the premise of the independence component should be correspondingly weakened; if it reflects irreversible fibrosis, the independence claim gains a stronger pathological basis. Future validation should attempt to separate these two components through imaging–histological correlation or longitudinal follow-up. This evidence derives from a review of fascial pathology, does not involve the posterior cervical region or forward head posture, and serves only to refine definitions; it does not constitute a direct test of the core hypothesis.

Three falsifiable components of the hypothesis:

First, the weight component. In individuals with long-standing FHP, the contribution weight of passive constraint from the deep sclerotic fibrous tissue of the dorsocervical hump to the maintenance of forward head posture is greater than the combined contribution of muscle imbalance and behavioral factors. The direct test of this component is undertaken by the joint model criterion (see Section 3.8 and Prediction 1); the mechanical threshold criterion does not by itself constitute proof of it.

Second, the independence component. Once sclerotic tissue has formed, it acquires mechanical independence relative to the original behavioral factors; its constraint effect does not depend on whether the original behavioral factors persist.

Third, the removal-effect component. After removal of the deep sclerotic fibrous tissue of the dorsocervical hump, the improvement in head position should be significantly greater than that after removal of an equal volume of non-sclerotic tissue, or significantly greater than that after rehabilitation training alone.

Fibrotic origins in the hypothesis: This hypothesis does not claim that sclerotic tissue must be the initiating factor of FHP. The origins of fibrosis and sclerosis are multi-pathway. Pathway A (behavioral secondary type): long-term head-down posture/FHP leads to chronic abnormal loading, which then promotes fibrosis and sclerosis; this is the traditional narrative. Pathway B (genetic dominant type): genetic susceptibility (relatively high fibroblast activity and enhanced tendency toward collagen deposition) allows sclerosis to form before FHP becomes obvious, and the sclerotic tissue, acting as a passive constraint, induces or aggravates FHP. Pathway C (environmental and metabolic induction type): chronic cold and damp exposure can promote fibrosis and sclerosis through local tissue hypoxia and inflammation; high-sugar and high-fat diet, obesity, and metabolic syndrome may participate in the formation of sclerotic tissue through chronic low-grade inflammation, insulin resistance, and increased collagen cross-linking. These factors can likewise induce or aggravate FHP as passive constraints.

A candidate molecular entry point for Pathway B is an imbalance in the TGF-β/BMP signaling axis: review-level evidence exists for the genetic and signaling regulation of this pathway in connective tissue diseases (6), and it can serve as a testable candidate pathway from genetic susceptibility to fibroblast activation and collagen deposition; however, no direct genetic testing of the deep sclerotic tissue of the dorsocervical hump is currently available. Human mechanistic references for Pathway C include the following: Béréziat et al. found non-inflammatory fibrosis in LMNA mutation-associated cervical adipose tissue, whereas mitochondrial DNA mutation-associated cervical lipoma manifests as inflammatory fibrosis (7), providing target-region corroboration that a pathological pathway independent of mechanical loading exists for posterior cervical fibrosis; however, that population consisted of patients with lipodystrophy rather than typical dorsocervical hump, and stiffness and head position were not measured. The above evidence supports only the mechanistic plausibility of multi-pathway origins and does not constitute a direct test of the core hypothesis.

The roles of genetic, environmental, and metabolic factors in Pathways B and C are based on general evidence from pan-fibrotic mechanisms; specific human studies targeting deep tissue sclerosis in the dorsocervical hump are currently lacking. In the hypothesis, they serve as theoretical background for multi-pathway origins, rather than as confirmed specific etiologies.

The comparison with behavioral factors in the weight component applies only to individuals in whom behavioral factors are still active; in individuals with a genetic-dominant type and very low behavioral exposure, this comparison reduces to whether passive constraint alone is sufficient to maintain forward posture, rather than whether passive constraint is greater than behavioral factors. In both circumstances, the core proposition holds, but the test design should be adjusted accordingly.

Regardless of the origin pathway of sclerotic tissue, the core proposition of this hypothesis is that in individuals with long-standing FHP, the deep sclerotic fibrous tissue of the dorsocervical hump already constitutes the main passive constraint on returning the head to a neutral position. The origins of fibrosis are multi-pathway, but its mechanical role in long-standing FHP is the same—a dominant passive constraint.

3. Literature-Based Evidence and Mechanical Reasoning Supporting the Hypothesis

One point warrants clarification at the outset. The following literature anchors several premises of the hypothesis rather than directly testing the core proposition itself. These premises include a measurable association between FHP and fascial stiffness, coexistence of posterior cervical structural changes with FHP, identification but not validation of stiffness as a maintaining mechanism, quantifiability of cervical fibrotic stiffness, ex vivo evidence for passive constraint of cervical flexion, anatomical continuity between the nuchal ligament and the spinal dura mater, finite element simulation of passive structure stress under FHP, layered anatomy of the posterior cervical fat pad, high SWE reliability, PIEZO2 expression in trapezius fascia, a fibrosis-dominant pathological subtype, concentration of nuchal ligament strain at C6/C7, absence of head-position outcomes in surgical systematic reviews, operative limitations from dense fibrous septa and deep fascial tethering, and the need for differentiated management of the fibrosis-dominant subtype. Other literature is used to reinforce the multi-pathway nature of origins, the quantitative benchmark for Prediction 4, the active muscle-side reference, the deep–superficial mechanical transmission pathway, the refinement of the definition of sclerosis, methodological control, and age calibration (see relevant sections below). The direct test of the core proposition is precisely the research direction called for in this article. This section focuses on evidence and reasoning at the mechanistic level and does not discuss specific surgical techniques or operative methods.

To reduce ambiguity about which level a given piece of literature supports, this article uses four evidence-citation levels. Level A denotes research that directly tests the core proposition; currently none exists, and this is precisely the research direction called for in this article. Level B denotes research that directly supports key premises, such as nuchal ligament resection experiments, SWE reliability studies, and studies demonstrating the existence of pathological subtypes. Level C denotes corroborating evidence from adjacent populations, adjacent tissues, or adjacent pathologies, used for mechanistic plausibility and not independently supporting the core proposition. Level D denotes literature on mechanistic background or definitional refinement, used for theoretical background and measurement definitions and not constituting empirical testing. The level is annotated at first citation in each section and is not repeated thereafter for conciseness.

3.1. In Vivo Evidence for FHP and Deep Tissue Stiffness of the Dorsocervical Hump

A study using SWE showed that in 16 healthy adults, the shear modulus of the nuchal fascia was significantly higher under forward head posture than under a neutral head position (P < 0.05), and the reliability of SWE for measuring nuchal fascial stiffness was moderate to excellent (ICC 0.63–0.89) (8). This study provides a direct in vivo signal for the sequence from change in head position to change in fascial mechanical properties. However, its measurement target was the nuchal fascia rather than the deep tissue of the dorsocervical hump, the sample included only 16 individuals, it measured acute posture-induced stiffness change rather than chronic structural sclerosis, and it used a cross-sectional design. These boundaries are referred to hereafter as the adjacent-evidence boundary of Liao 2023.

Regarding measurement reliability, a 2025 study reported higher test–retest reliability for the posterior cervical fascia: ICC(3,1) ≥ 0.90, with reliability ≥ 0.80 for fascial thickness and the fascia/subcutaneous fat stiffness ratio (9). That study included patients with chronic neck pain and healthy controls, directly measured the posterior cervical fascia, and simultaneously measured subcutaneous fat stiffness to calculate a ratio. This design corresponds directly to the requirement in this article to test the independent effect of sclerosis after controlling for fat pad thickness. This reliability level is higher than the ICC 0.63–0.89 reported by Liao 2023 and can be preferentially cited as the methodological basis for SWE as a core measurement tool.

Regarding target specificity, a 2026 study published in Aesthetic Plastic Surgery performed Masson staining and ImageJ collagen quantification on surgical specimens from 86 patients with dorsocervical fibrofatty prominence and, using K-means clustering, identified three subtypes: a fat-dominant subtype (collagen content <23.3%), a mixed subtype (23.3–38.4%), and a fibrosis-dominant subtype (>38.4%) (4). This is currently the only pathological study that directly uses specimens from patients with dorsocervical hump and demonstrates at the patient-population level that a fibrosis-dominant subtype exists objectively. It provides pathological gold-standard support for the core operational distinction in this article: sclerosis independent of fat volume. Boundaries: this was a cross-sectional pathological classification that did not measure forward head posture and did not involve mechanical constraint; moreover, the accuracy of SWE in distinguishing fibrotic subtypes was only 48.0%–67.2%, lower than the 92%–93% of B-mode ultrasound (4), suggesting that SWE measurement of sclerosis in the dorsocervical hump region requires cautious interpretation.

Regarding anatomical layering and fibrous tissue evidence of the posterior cervical fat pad, a human cadaveric anatomical and histological study confirmed by histological staining that the posterior cervical fat pad consists of superficial and deep adipose layers (2). Reference (2) demonstrates that the posterior cervical fat pad has two anatomical layers, superficial and deep—a finding that provides direct support for deep tissue being an independently localizable anatomical component; however, it does not demonstrate that the deep layer is fibrosis-dominant, which would require a study directly comparing collagen density between the superficial and deep layers for confirmation. Reference (3), in turn, demonstrates that fibrous connective tissue in the dorsocervical region is more prominent than in the abdomen, supporting the notion that fibrous tissue exists independently of fat volume. Taken together, the two support the notion that deep tissue can be independently localized and dorsocervical fibrous connective tissue is more prominent, rather than that the deep layer is fibrosis-dominant. Boundaries: neither study was conducted specifically in patients with dorsocervical hump, and neither measured tissue stiffness nor head position; Reference (2) was a cadaveric dissection with a limited sample size.

In addition, a 2026 systematic review and meta-analysis published in Aesthetic Plastic Surgery defined dorsocervical hump as dorsocervical fibro-lipodystrophy, explicitly establishing at the level of disease nomenclature that its fibrous component is independent of simple fat accumulation, and, when pooling surgical outcomes, used recurrence and complications as the main outcome domains (10). This is not a mechanical outcome study, but at the systematic-review level it confirms that a fibrous component requiring specific management exists within the dorsocervical hump region, consistent with the core distinction in this article that deep sclerotic fibrous tissue is an independent component.

At the operative level, a study on ultrasound-assisted liposuction for idiopathic dorsocervical hump explicitly noted that dense fibrous septa and deep fascial tethering in the posterior cervical region can limit liposuction results: even with energy-assisted techniques and adequate aspiration volume, deep tissue may remain dense, fixed, and resistant to cannula passage, resulting in relative undercorrection (11). This confirms, from a surgical perspective, that fibrous tissue is a mechanical component that requires independent identification and constitutes a source of operative resistance. Boundaries: this was a small-sample retrospective study that did not measure tissue stiffness and did not involve head position; it supports only the independent existence and operative weight of fibrous tissue. In addition, for fibrosis-dominant dorsocervical hump, the TABLE technique uses a limited open approach and explicitly takes the limitations of conventional minimally invasive techniques in the fibrosis-dominant subtype as its starting point; this provides indirect surgical-strategy support for the notion that the fibrosis-dominant subtype is a mechanical entity requiring independent identification (12). Boundaries: this was a retrospective case series whose main outcomes were contour improvement and patient-reported cervical extension range of motion; it did not measure tissue stiffness or forward head angle and cannot demonstrate that removal of sclerotic tissue improved head position.

Regarding deep–superficial mechanical coupling, anatomical and imaging studies describe posterior cervical adipose tissue as interwoven by thick, vertically oriented fibrous septa that are firmly anchored to the deep cervical fascia and nuchal ligament; dense fibrous septa and deep fascial tethering are regarded as anatomical limiting factors for contour correction in the posterior cervical region. This provides a concrete structural pathway for the notion that sclerosis or contracture of the deep investing fascia or nuchal ligament can be transmitted through fibrous septa as traction on the superficial fat pad and surrounding tissues. Boundaries: this evidence is anatomical/imaging description that did not measure stiffness, did not involve forward head posture, and did not provide quantitative mechanical data; anchoring is a morphological fact and does not imply that anchoring tension necessarily increases under sclerotic conditions. It supports the existence of a structural pathway but does not prove the weight of this pathway in the maintenance of FHP.

At the level of soft tissue biology, chronic mechanical loading promotes fibrosis and sclerosis through a microinjury–inflammation–fibroblast activation–collagen deposition pathway, which is a known pathophysiological process. Under forward head posture, the C7–T1 junction and the posterior cervical fascia are continuously subjected to abnormal traction and flexion stress, providing the mechanical conditions for this pathway. However, the existing literature lacks human longitudinal evidence for the progression from chronic FHP to deep structural sclerosis of the dorsocervical hump; sclerosis itself is affected by multiple factors such as metabolism, age, and hormone levels, and should not be reduced to a single mechanical causation.

The above evidence supports the premises of the hypothesis—that an independently localizable deep tissue exists in the posterior cervical region, that dorsocervical fibrous connective tissue is more prominent, that chronic loading can promote fascial sclerosis, and that the fibrosis-dominant subtype requires differentiated management—but not the core proposition itself, which has not yet been directly tested.

3.2. Coexistence of Posterior Cervical Structural Changes and FHP

A cephalometric study involving 256 participants showed that the craniocervical angle in the ossification of the nuchal ligament (ONL) group was significantly greater than that in the control group, indicating that ONL is associated with more pronounced forward head posture (13). This is an independent corroboration, in a relatively large sample, of the coexistence of posterior cervical structural changes and FHP. This study suggests that posterior cervical structural changes can coexist with FHP; the deep sclerotic fibrous tissue of the dorsocervical hump belongs to a structural change in the same anatomical region, but the pathological type (ossification vs. fibrotic sclerosis) differs, and the two cannot be directly equated. Moreover, this study used a cross-sectional design and cannot determine the direction of causality. Its reasonable use in the hypothesis is to show that once an irreversible change occurs in a posterior cervical structure, that structure can form a stable co-localized relationship with FHP. This provides corroboration from an adjacent pathological type for the claim that sclerotic tissue acquires mechanical independence, but it cannot replace direct evidence regarding the deep sclerotic tissue of the dorsocervical hump itself.

At the level of clinical narrative, a narrative review framed around Text Neck Syndrome reported a patient with long-term mobile phone use (10 hours/day) accompanied by loss of cervical lordosis and ONL at the C4/C5 level; the authors presented this coexistence as a hypothesis-generating observation that long-term device use and forward head posture may constitute mechanical triggers (14). The article explicitly acknowledged that postural parameters were not formally measured and that causality could not be inferred; its value lies in providing a descriptive footnote for the clinical association between behavioral exposure and structural change, rather than in providing mechanical evidence. Its pathological type (ossification) and target region (C4/C5) also differ from the core object of this article (C7/T1 fibrotic sclerosis).

3.3. Theoretical Framework for Stiffness as a Maintaining Mechanism

A 2026 narrative review proposed that persistent cervicothoracic mechanical stiffness may serve as a time-dependent mechanism linking postural loading to chronic neck pain (15). This article closely parallels the present hypothesis in logic (from loading to stiffness to symptom maintenance), but it repeatedly emphasizes that direct cervicothoracic evidence in patients with chronic neck pain remains limited and that direct longitudinal evidence validating this pathway remains limited. The value of citing this article lies not in providing original evidence but in illustrating that the idea of stiffness as a maintaining mechanism has already been identified in the literature while its direct testing remains a blank space. The present hypothesis points precisely to this identified but unfilled gap.

This article focuses on muscle mechanical stiffness rather than fascial fibrotic sclerosis; the value of its conceptual model lies in suggesting the framework of time-dependent maintenance, but extending it to the fascial level and assigning it the mechanical weight of a dominant passive constraint is precisely the gap identified by the present hypothesis.

3.4. Quantitative Reference for the Degree of Sclerosis in Human Cervical Fibrotic Tissue

A 2026 study published in Physics and Imaging in Radiation Oncology used SWE to quantify tissue-specific stiffness of radiation-induced cervical fibrosis after head and neck cancer radiotherapy. The study included 16 patients with bilateral cervical lymphatic irradiation and 16 age-, sex-, and body mass index (BMI)-matched non-irradiated controls; fascial stiffness was significantly higher in the irradiated group than in controls (left side 46.41 vs. 25.47 kPa; right side 44.28 vs. 22.69 kPa) (16). This study demonstrates that the degree of sclerosis in human cervical fibrotic tissue can be quantified by SWE and that stiffness is significantly higher than that of normal tissue. Two boundaries warrant attention: first, the stiffness difference in subcutaneous tissue is far less pronounced than that in muscle and fascia, which precisely supports the core distinction in this article that sclerosis is located mainly in deep fascia/fibrous tissue rather than in superficial fat; second, despite the significant increase in tissue stiffness, there was no significant between-group difference in cervical range of motion, suggesting that a dissociation may exist between increased fibrotic stiffness and functional limitation (16).

This study contains a finding that creates tension for the present hypothesis: although fascial stiffness was significantly increased (approximately 1.8-fold), there was no significant difference in cervical range of motion between the irradiated group and controls (16). This phenomenon of increased stiffness–functional limitation dissociation requires a direct response rather than dismissal merely on the grounds of population mismatch. To avoid post hoc justification, this article first establishes a discriminant framework and then offers explanations. If future direct measurements in individuals with dorsocervical hump reveal that head-position metrics correlate with the stiffness of deep sclerotic tissue while composite cervical range of motion does not, this would support the focal directional constraint explanation, and the weight component would not be refuted. If head-position metrics also do not correlate with stiffness, the weight component would face direct refutation. If pain, atrophy, or age indicators explain most of the variance, alternative explanations would take precedence, and the sclerosis effect would need to be re-examined after controlling for these indicators.

Under this framework, four possible explanations exist, and the present hypothesis relies on the first two:

First, the mechanical behavior of diffuse versus focal fibrosis differs. Radiation-induced fibrosis involves all layers—skin, subcutaneous tissue, muscle, and fascia—with collagen deposition distributed relatively isotropically across directions, forming a diffuse stiffness rather than a directional tension band. In the dorsocervical hump, however, deep sclerotic tissue may form focal, oriented fibrous bands along the course of the investing fascia and fibrous septa, generating a concentrated passive flexion moment in the sagittal flexion direction. The restriction of multi-segmental composite range of motion by isotropic diffuse stiffness may be offset by compensation from adjacent segments, whereas the constraint imposed by a focal oriented tension band on a specific direction (sagittal head-position maintenance) is more difficult to compensate for.

Second, range of motion is a multi-segmental composite measure, whereas head-position maintenance is a single-dimensional directional measure. Dapper et al. measured overall cervical range of motion (possibly a composite of flexion–extension, lateral bending, and rotation), and a directional constraint at one segment (C7–T1) may be masked by compensatory hypermobility of the upper cervical spine (C0–C2). The craniovertebral angle measures sagittal head position and is more sensitive to a directional constraint at the C7–T1 junction. In other words, normal range of motion does not equal unrestricted head-position maintenance—this is precisely the reason why Prediction 1 in this article selects the craniovertebral angle rather than range of motion as the primary outcome.

Third, post-radiation tissue may simultaneously exhibit atrophy and fibrosis. Radiation can cause muscle atrophy and skin thinning, and the laxity resulting from atrophy may offset the stiffness resulting from fibrosis, leaving net range of motion unchanged. The dorsocervical hump region does not have an equivalent degree of radiation-induced atrophy, and the net mechanical effect of the sclerotic band may manifest more purely as increased constraint.

Fourth, pain-related protective inhibition may confound range-of-motion measurement. Post-radiation patients often have pain and muscle inhibition, which may limit the full expression of active range of motion and mask the mechanical effect of fibrosis through pain behavior. The pain burden in the dorsocervical hump population is usually lighter, and the mechanical effect of the sclerotic band may be more directly exposed.

Among the above explanations, the first two can be directly absorbed by the present hypothesis—they convert Dapper's negative finding from a refutation into a boundary condition: increased stiffness does not necessarily lead to decreased multi-segmental range of motion, but may constitute a constraint in the unidimensional, directional dimension of head-position maintenance. The latter two are alternative explanations that need to be controlled in validation by incorporating pain and atrophy indicators. Under the above discriminant framework, if future direct measurements in individuals with dorsocervical hump reveal that the stiffness of deep sclerotic tissue is significantly increased but the craniovertebral angle is unrelated to stiffness, then the weight component of the present hypothesis would face direct refutation. This refutation condition is closer to the target than Dapper's post-radiation data.

3.5. Ex Vivo Biomechanical Evidence for the Constraint of Cervical Flexion by Posterior Passive Structures

A biomechanical study conducted on 12 human cervical spine specimens directly measured changes in cervical range of motion before and after nuchal ligament resection. The results showed that after nuchal ligament resection, cervical flexion range of motion immediately increased by 28% and tangent stiffness decreased by 27%, both reaching statistical significance (17). This provides direct ex vivo experimental evidence for the premise that posterior cervical passive structures are an important mechanical constraint limiting cervical flexion. Boundaries: the measurement target was the normal nuchal ligament rather than pathological sclerotic tissue, and the experimental condition was ex vivo specimens rather than living individuals with FHP. However, it biomechanically demonstrates a key premise: the stiffness of posterior cervical passive structures can substantially affect the flexion range of the cervical spine. If the normal nuchal ligament can contribute approximately 27% of flexion stiffness, then it is fully reasonable that an abnormally sclerotic and thickened fibrous band would produce greater passive constraint mechanically.

At the strain-distribution level, the narrative review by Chiang and Chu (2026) explicitly stated that the lower segment of the nuchal ligament, especially its attachment sites at C6 and C7, bears peak mechanical strain during cervical flexion; the article further proposed that chronic repetitive traction microtrauma at these fiber–bone junctions is a key mechanism triggering heterotopic ossification (14). This provides secondary synthesized evidence at the strain-distribution level for the premise in this article that abnormal loading in chronic FHP is concentrated at the cervicothoracic junction. Boundaries: this is a narrative review, not an original biomechanical measurement study; its statement regarding peak strain at C6/C7 cites earlier literature.

3.6. Anatomical Continuity Between the Nuchal Ligament and the Spinal Dura Mater

A human anatomical study published in PeerJ observed, through fine dissection, fibrous continuity between the nuchal ligament and the spinal dura mater and noted that passive cervical motion can stretch these ligamentous connections (18). This provides a direct morphological basis for the notion that nuchal ligament tension can be transmitted to deep structures. Boundaries: this is an anatomical description that does not involve FHP, fibrosis, or head-position maintenance, and the specimen source was cadaveric dissection. It supports only the anatomical possibility of a mechanical transmission pathway and does not constitute direct support for the core hypothesis (that sclerotic tissue is a dominant passive constraint).

Continuity between the nuchal ligament and the spinal dura mater remains controversial. A 2026 review published in Frontiers in Medicine systematically reviewed the morphological evidence for the myodural bridge complex and pointed out that method-dependent observational discrepancies exist in this field: some studies confirmed continuity only at the upper cervical level, and whether the continuity is sufficiently dense and whether it extends downward to the mid-to-lower cervical spine remain controversial (19). Therefore, when citing (18), this article must exercise restraint: the mechanical weight of this pathway should not be over-extrapolated. This evidence conflict does not affect the core hypothesis of this article—the core hypothesis relies on the constraint of cervical flexion by posterior passive structures (Section 3.5) and the mechanical consequences of sclerotic tissue (Section 3.8), rather than on the nuchal ligament–spinal dura mater continuity itself.

3.7. Computational Simulation of Passive Structure Stress Under FHP by Whole-Cervical Finite Element Models

A 2026 study published in the Journal of the Mechanical Behavior of Biomedical Materials used a literature-validated whole-cervical finite element model (C0–T1) to systematically simulate the biomechanical effects of forward head posture on cervical structures. The results showed that FHP leads to increased upper cervical lordosis and decreased lower cervical curvature, accompanied by measurable narrowing of the neural foraminal space and elevated cortical bone stress; the model was able to analyze the stress and strain distribution of passive structures such as ligaments under FHP (20). This is methodologically complementary to the ex vivo experimental evidence in Section 3.5: one comes from ex vivo experiments and the other from computational simulation, together providing a complementary evidence chain for the premise that posterior cervical passive structures bear and transmit significant mechanical loads in FHP. Boundaries: this is a computational simulation study, and its conclusions depend on the ligament material properties and geometric parameters specified in the model; moreover, it simulates the response of normal ligaments under abnormal posture rather than the mechanical behavior of pathological sclerotic tissue.

3.8. Mechanical Reasoning for Sclerotic Fibrous Tissue as a Passive Constraint

The following reasoning is a mechanical plausibility argument. Its function is to demonstrate the mechanical validity of the proposition that if sclerotic tissue is sufficiently stiff, head position can be locked by passive constraint; it does not constitute a direct test of the core proposition.

From a mechanical perspective, if the deep sclerotic fibrous tissue of the dorsocervical hump forms a passive tension band with markedly reduced elasticity, this tissue can generate a passive flexion moment aligned with the forward direction of head posture when the cervical spine attempts to return to a neutral position. In the sagittal plane force balance of the cervical spine, head position is maintained jointly by active muscle forces (deep cervical flexors and posterior cervical extensors) and passive structures (ligaments, fascia, intervertebral discs). Existing evidence supports the mechanical role of passive structures in FHP from multiple angles. The ex vivo experiment in Section 3.5 shows that the normal nuchal ligament can contribute up to 27% of flexion stiffness. The computational simulation in Section 3.7 shows that passive structures bear quantifiable stress and strain under FHP. The anatomical study in Section 3.6 suggests that nuchal ligament tension can be transmitted deeply along anatomical continuity. The post-radiation fibrosis data in Section 3.4 suggest that the stiffness of pathologically fibrotic fascia can reach approximately twice that of normal tissue (16). Similarly, the SWE reliability study cited in Section 3.1 demonstrates that the stiffness ratio of fascia to subcutaneous fat can be reliably measured (9), providing an operable methodological premise for separating the mechanical contributions of sclerotic tissue and fat pad in vivo. The pathological classification study cited in the same section demonstrates that a fibrosis-dominant subtype with collagen content >38.4% exists objectively in patients (4). The description of nuchal ligament strain distribution cited in Section 3.5 indicates that strain during flexion is concentrated at the C6/C7 attachment sites (14). The layered anatomical study cited in Section 3.1 demonstrates that the posterior cervical fat pad has a superficial and a deep layer (2). If the stiffness of the deep sclerotic tissue of the dorsocervical hump is also significantly higher than that of the normal nuchal ligament, then the active muscle force must overcome greater passive resistance to bring the head back to a neutral position. When the passive resistance exceeds the range that active muscle force can compensate for, head position becomes locked in the forward position.

Simplified order-of-magnitude estimation. The following estimation is intended to illustrate that the passive contribution of the sclerotic band may be non-negligible in order of magnitude and is not a precise calculation; it answers only whether it may be non-negligible, not whether it is actually large enough, and does not constitute an empirical test of the core proposition.

Let the total stiffness of normal posterior cervical passive structures to flexion be KpassiveKpassive. The ex vivo experiments of Takeshita et al. (17) showed that after resection of the normal nuchal ligament, cervical flexion tangent stiffness decreased by 27%, indicating that the normal nuchal ligament contributes approximately 0.27Kpassive0.27Kpassive. Dapper et al. (16) reported that the shear modulus of post-radiation fibrotic fascia was approximately 1.8 times that of normal tissue (46.41 vs. 25.47 kPa on the left side). If the stiffness of the deep sclerotic band of the dorsocervical hump is also approximately 1.8 times that of the normal nuchal ligament, and if its mechanical role in sagittal flexion constraint is comparable to that of the nuchal ligament (a simplifying assumption), then the flexion stiffness contribution of this sclerotic band would be approximately 0.27×1.8≈0.49Kpassive0.27×1.8≈0.49Kpassive, that is, approximately 0.22Kpassive0.22Kpassive higher than the contribution of the normal nuchal ligament.

This increment implies that the active muscles (deep cervical flexors and posterior cervical extensors) would need to overcome additional passive resistance equivalent to approximately 81% (0.22/0.27) of the original nuchal ligament contribution. Overcoming this resistance would be necessary to bring the head from a forward posture back to a neutral position. If the maximum flexion–extension moment reserve of the active muscles is insufficient to cover this increment, head position becomes locked in the forward position. Suzuki et al. (21) reported that upper trapezius stiffness explains only approximately 11% of the variance in FHP, and Blomgren et al. (22) reported that deep cervical flexor training is ineffective for strength and endurance under high load—these two active-side references suggest that the compensatory reserve of the active muscles may not be ample. Therefore, the order of magnitude indicated by a doubling of sclerotic band stiffness, with an approximately 80% increase in passive resistance, is mechanically sufficient to constitute a non-negligible constraint weight.

This estimation has three limitations. The value 0.27 derives from normal nuchal ligament resection experiments and cannot be directly extrapolated to the mechanical contribution of the sclerotic band; the 1.8-fold value derives from post-radiation fibrosis and cannot be directly extrapolated to sclerotic tissue in dorsocervical hump; and equating the sclerotic band with the mechanical role of the nuchal ligament is a strong simplification. The function of this estimation is only to illustrate that it may be large enough in order of magnitude, not to prove that it is actually large enough; the precise weight must be tested through the cross-sectional independent prediction in Prediction 1 and the early-versus-late difference in Prediction 4.

Two criteria for dominance. This article operationalizes dominance as two parallel criteria that serve different functions and cannot substitute for each other. The first is the mechanical threshold criterion, a necessary but not sufficient condition. The threshold is met when the flexion stiffness contribution of the sclerotic band exceeds 1.5 times that of the normal nuchal ligament—approximately 0.40 times the total stiffness of normal posterior cervical passive structures. This threshold is an operational convention, not a natural constant; its function is to convert cross-sectional stratification from a qualitative comparison into a comparable numerical judgment. Meeting this threshold does not mean that the weight component has been proven, because its comparison target is normal passive structures rather than muscle and behavioral factors. The second is the joint model criterion, which constitutes a direct test of the weight component: in Prediction 1, head-position metrics are used as the dependent variable; with fat pad thickness included as a covariate, sclerosis severity, muscle function, and behavioral factors are simultaneously entered into the model. If the independent explanatory power of sclerosis severity exceeds the combined explanatory power of muscle and behavioral factors, the weight component receives direct support; if it does not exceed that combined explanatory power, the weight component is refuted. The mechanical threshold and the joint model are two test pathways for the same proposition: the former is used for cross-sectional stratification, and the latter for weight comparison. The order-of-magnitude estimation serves only the plausibility argument of whether the mechanical threshold may be reached and does not serve the empirical test of whether the weight component holds. This distinction can avoid the circular appearance of using the estimation to prove the threshold and using the threshold to explain the estimation.

This order-of-magnitude estimation and the boundary condition in Section 3.4 are two sides of the same argument: Section 3.4 shows that increased stiffness does not necessarily manifest as decreased multi-segmental range of motion, and Section 3.8 shows that in the unidimensional directional domain of head-position maintenance, an increment of 0.22Kpassive0.22Kpassive is sufficient to constitute a non-negligible passive resistance. Together, the two define the applicable dimension of dominance—not composite range of motion, but sagittal head-position maintenance.

The key point is that the mechanical contribution of sclerotic fibrous tissue does not depend on muscle weakness. Even with normal deep cervical flexor strength, head position may remain forward if passive tension-band stiffness is sufficiently high. This explains why muscle training alone has limited effects in some individuals with long-standing FHP: it does not relieve the passive constraint. A quantitative reference from the active side can further illustrate this weight issue: a study conducted in 40 young men used SWE to measure the shear elastic modulus of the upper trapezius and found only a weak negative correlation with the craniovertebral angle (ρ = −0.338), meaning that upper trapezius stiffness can explain only approximately 11% of the variance in FHP severity (21). In addition, a systematic review of 12 RCTs reported that deep cervical flexor training can improve neuromuscular coordination and head–neck posture but is ineffective for strength and endurance under high load, with limited or contradictory evidence for effects on other functional outcomes (22). These two lines of evidence together suggest that active-side training targeting muscle imbalance may have a definite ceiling in its effects. This does not prove passive constraint dominance, but it provides an active-side reference for the weight component of the hypothesis: if the association between active muscle stiffness and FHP is so weak and the effects of active-side training are so limited, then the traditional narrative attributing FHP maintenance mainly to muscle factors itself requires quantitative evidence of the same magnitude. Boundaries: the measurement target was muscle rather than fascia; the design was cross-sectional and cannot determine causality; the sample consisted of young men, limiting extrapolation.

3.9. Biological Plausibility of Multi-Pathway Origins

Genetic susceptibility in fibrosis has general supporting evidence: individuals differ in their fibrotic response threshold to mechanical loading, and fibroblast activity and the tendency toward collagen deposition are influenced by genetic variation. This explains why, under the same postural loading, only some individuals develop a prominent dorsocervical hump and deep sclerotic tissue.

At the level of mechanotransduction, a 2026 study detected PIEZO2 expression in the human trapezius fascia and further showed that Pacinian- and Ruffini-like mechanoreceptor structures are present in this fascia (23). The trapezius fascia is precisely the layer formed by the investing fascia at the cervicothoracic junction as it wraps posteriorly around the trapezius, corresponding anatomically and directly to the target region of the hypothesis. This provides a direct human histological anchor for the capacity of posterior cervical fascial fibroblasts to perform mechanotransduction. Boundaries: the study did not directly measure the degree of fibrosis or stiffness and cannot establish a causal chain between mechanotransduction and sclerosis in this region.

More importantly, increased tissue stiffness itself can generate a profibrotic positive-feedback loop through mechanotransduction: He et al. (2024) demonstrated in a skin fibrosis model that increased matrix stiffness can drive further collagen deposition and progressive sclerosis through a Piezo1–Wnt2/Wnt11–CCL24 positive feedback loop (24). This provides a testable candidate molecular mechanism for the independence component of this article: sclerosis is not only a passive tension band but may also be a self-reinforcing pathophysiological process. Boundaries: the tissue source in that study was skin rather than posterior cervical fascia, and the findings cannot be directly extrapolated to the mechanism of deep sclerosis in dorsocervical hump.

This stiffness-to-fibrosis positive feedback is not unique to a single pathway. Otto and Klingler (2026), within a fascial biology framework, systematically reviewed how two mechanotransduction axes—TGF-β1/Smad2/3 and Piezo1/YAP/TAZ—converge on collagen deposition and extracellular matrix (ECM) stiffening, and explicitly described this as a self-amplifying fibrotic feedback loop (25). Boundaries: the context of that review was tumor-associated fascial remodeling, not posterior cervical investing fascia, and it did not involve forward head posture.

Regarding environmental and metabolic factors, chronic cold and damp exposure can activate fibroblasts and promote collagen deposition through vasoconstriction, local hypoxia, and release of inflammatory cytokines; high-sugar and high-fat diet, obesity, and metabolic syndrome may participate in the formation of sclerotic tissue through chronic low-grade inflammation, insulin resistance, increased advanced glycation end products (AGEs), and enhanced collagen cross-linking. Fascial pathology lists trauma, surgery, diabetes, and aging as independent triggers of fibrosis, whereas diet and overuse mainly lead to reversible densification (5). This provides direct theoretical support from fascial biology for the independent role of metabolic factors (diabetes, high-sugar and high-fat diet) in Pathway C, and at the same time suggests that behavioral postural loading (overuse) and metabolic factors may affect tissue stiffness through two different pathways—densification and fibrosis, respectively. Béréziat et al. (2011) found non-inflammatory fibrosis in LMNA mutation-associated cervical adipose tissue (7), providing corroboration from cervical tissue for the existence of a pathological pathway of posterior cervical fibrosis independent of mechanical loading; however, that population consisted of patients with lipodystrophy rather than typical dorsocervical hump. The above literature collectively supports the notion that fibrosis and sclerosis have multi-pathway origins, but cannot replace direct human studies of deep investing fascial sclerosis in dorsocervical hump.

The genetic, environmental, and metabolic pathways and the behavioral pathway are not mutually exclusive: genetically susceptible individuals may develop sclerosis even under relatively low behavioral loading; individuals with environmental exposure or metabolic dysregulation may already have sclerosis when behavioral loading is not high; and the four categories of factors may act synergistically. This multi-pathway model enables the hypothesis to accommodate clinical heterogeneity without relying on the fragile premise that behavioral factors must come first.

4. Testable Predictions

If the hypothesis holds, the following predictions should be observed:

Prediction 1 (weight prediction): In individuals with long-standing FHP, the shear modulus of the deep sclerotic fibrous tissue of the dorsocervical hump measured by SWE should predict the severity of forward head posture independently of muscle function indicators, fat pad thickness, and behavioral factors (screen time, physical activity level). That is, after controlling for fat pad thickness, muscle function, and behavioral factors, sclerosis severity should still explain a significant proportion of the variance in forward head posture. According to the joint model criterion in Section 3.8, the independent explanatory power of sclerosis severity should exceed the combined explanatory power of muscle and behavioral factors. This comparison is operationalized as the incremental variance in head-position metrics explained by sclerosis severity after entering fat pad thickness, muscle function, and behavioral factors. This incremental variance should exceed the variance explained jointly by muscle function and behavioral factors. The interpretation of a positive or null association between head-position metrics and stiffness follows the discriminant framework in Section 3.4. The testability of this prediction depends on the reliable separate measurement of fascial stiffness and subcutaneous fat stiffness—the SWE reliability study cited in Section 3.1 has already demonstrated reliability ≥ 0.80 for the fascia/subcutaneous fat stiffness ratio (9). At the same time, given that the accuracy of SWE in distinguishing fibrotic subtypes in patients with dorsocervical hump is limited (4), the study design may first use B-mode ultrasound fibrosis scoring for subtype stratification and then quantify stiffness with SWE within strata. The validity of this prediction presupposes that SWE has discriminative validity in the long-standing FHP population; if this premise does not hold, B-mode ultrasound fibrosis scoring should be used as the primary stratification variable and SWE only as a secondary quantitative indicator, with Prediction 1 correspondingly downgraded to the prediction that fibrosis scoring independently predicts forward head posture beyond fat pad thickness, muscle function, and behavioral factors.

Prediction 2 (independence prediction): In individuals whose original behavioral factors (such as screen time) have been reduced or eliminated, if sclerotic tissue has already formed, forward head posture should not fully correct; its residual severity should correlate with the shear modulus of the deep tissue of the dorsocervical hump rather than with current behavioral factors.

Prediction 3 (removal-effect prediction): Under rigorously controlled conditions, an intervention that removes the deep sclerotic fibrous tissue of the dorsocervical hump should produce a significantly greater improvement in head position than at least one of the following comparators: rehabilitation training of equivalent intensity; or, where ethically and practically feasible, removal of an equal volume of non-sclerotic tissue. Moreover, the magnitude of improvement should correlate positively with the preoperative shear modulus of that tissue. Prediction 3 tests the effect of the mechanical operation of removing sclerotic tissue, not that of any specific procedure; the choice of procedure is an execution detail of the validation pathway (Section 5.2) and is not discussed at the level of the hypothesis. Where ethically and practically feasible, the comparator should include removal of an equal volume of non-sclerotic tissue; otherwise, rehabilitation training of equivalent intensity serves as the comparator. To make this prediction executable, validation must prespecify criteria for removal of sclerotic tissue rather than simple fat: the target tissue should be defined preoperatively by SWE stiffness and B-mode fibrosis scoring, the extent of fibrous septa and investing fascia addressed should be recorded intraoperatively, and collagen quantification should be performed on specimens when available postoperatively; the primary analysis should be restricted to cases in which removal of sclerotic tissue is confirmed. If sclerosis consists mainly of reversible densification, conservative fascial intervention may partially relieve the passive constraint, and Prediction 3 would then be downgraded to the prediction that conservative fascial intervention should partially improve head position and that the improvement should correlate with baseline stiffness; if irreversible fibrosis predominates, the removal-effect prediction would be maintained. The validation design should attempt to separate the two components through imaging–histological correlation or longitudinal follow-up and to stratify the analysis of the magnitude of the removal effect accordingly.

Prediction 4 (early-versus-late difference prediction): Prediction 4 is a composite test of the weight component and the independence component, but the refutation conditions for the two components should be specified separately: if the training effect in individuals with established sclerosis is significantly lower than that in early-stage individuals, this would indicate that the weight of passive constraint increases with the formation of sclerosis (weight component) and that this constraint is not relieved by training targeting the active side (independence component). In early-stage FHP individuals in whom sclerotic tissue has not yet formed, posture correction training should effectively improve head position; in long-standing FHP individuals in whom sclerotic tissue has already formed, the effect of posture correction training alone should be significantly smaller than that in early-stage individuals, whereas interventions combined with relief of passive constraint should show greater effects. The quantitative benchmark for this prediction is as follows: Xing et al. (2026) reported a pooled SMD of 0.95 (95% CI 0.61–1.28) for therapeutic exercise improving the craniovertebral angle in patients with FHP and neck pain, with low to moderate certainty of evidence (1). If the training effect in late-stage individuals with established sclerosis is not significantly lower than that in early-stage individuals (with the pooled estimate of 0.95 used only as an external benchmark for whether the late-stage effect is meaningfully low), the weight component of the present hypothesis of passive constraint dominance would face direct refutation; however, whether the independence component is refuted still needs to be determined by the results of Prediction 2. The refutation logic is as follows: if the training effect in late-stage individuals is significantly lower than that in early-stage individuals, the result would support both the weight component and the independence component. If the training effect does not differ between late- and early-stage individuals, the weight component would be refuted, and the independence component would require separate testing by Prediction 2. If residual forward head posture after elimination of behavioral factors correlates with current behavior rather than with stiffness, the independence component would be refuted. Only when both the weight component and the independence component are simultaneously refuted would a joint refutation of the core proposition be constituted. This pooled estimate has published methodological controversies (inconsistent inclusion criteria, high heterogeneity, limited statistical power of subgroup analyses), and the robustness of its use as a refutation anchor needs to be considered in interpretation.

5. Validation Pathways

5.1. Tier 1: Cross-Sectional Association and Independent Prediction

In a population with long-standing FHP, simultaneously measure deep tissue stiffness of the dorsocervical hump (SWE), fat pad thickness (ultrasound), head-position metrics (craniovertebral angle, C0–C2 angle, sagittal vertical axis offset), muscle function (deep cervical flexor endurance, surface electromyography [sEMG]), and behavioral factors. Using head-position metrics as the dependent variable, test the independent explanatory power of deep tissue stiffness after controlling for fat pad thickness, muscle function, and behavioral factors (Prediction 1); in the subgroup in which behavioral factors have been reduced, test whether residual forward head posture correlates with deep tissue stiffness rather than with current behavior (Prediction 2). The measurement protocol should preferentially adopt methods that can simultaneously acquire fascial and subcutaneous fat stiffness and calculate their ratio (9). Given that the accuracy of SWE in distinguishing fibrotic subtypes in the dorsocervical hump region is limited (4), concurrent acquisition of B-mode ultrasound fibrosis scoring is recommended as a subtype stratification variable. All SWE measurements should be performed under standardized head–neck posture and resting muscle conditions, and age should be recorded to assess age-related changes in elasticity.

We operationalize long-standing FHP with a dual definition: at enrollment, by exposure duration or behavioral exposure amount—for example, years of screen use and average daily head-down time—with specific thresholds fixed in preregistration; at stratification, by sclerosis severity rather than by disease duration alone. The primary analysis uses stratification by sclerosis severity to avoid defining exposure by outcome; disease duration serves only as a secondary stratification variable. The above measurement protocol should fix the primary outcome, SWE measurement level, and stratification rules in preregistration; assessors should be blinded to head-position metrics and group assignment; and sample size should be estimated based on SWE reliability and the minimal detectable change (MDC) from pilot data rather than determined post hoc. If pilot testing shows that the test–retest reliability of SWE in the dorsocervical hump region is below ICC 0.80 or that its agreement with B-mode fibrosis scoring is insufficient, the primary stratification variable should be changed to B-mode fibrosis scoring, with SWE used only as a secondary quantitative indicator; this downgrade rule should be prespecified in the preregistration.

5.2. Tier 2: A Controlled Study Separating Relief of Passive Constraint From Rehabilitation Effects

Patients with long-standing FHP who meet the indication criteria are randomly assigned to a group receiving an intervention that relieves the passive constraint of the deep sclerotic tissue of the dorsocervical hump plus standardized rehabilitation or to a standardized rehabilitation group. Where ethically and practically feasible, a third comparator involving removal of an equal volume of non-sclerotic tissue should be included; otherwise, the standardized rehabilitation group serves as the comparator. The primary outcome is change in head-position metrics; secondary outcomes are change in deep tissue stiffness, change in fat pad thickness, and muscle function. Test whether the improvement in head position in the intervention group is significantly greater than at least one of the following: that in the rehabilitation group; or, when a non-sclerotic tissue comparator is included, that in the comparator group (Prediction 3). Also test the correlation between the magnitude of improvement and the preoperative shear modulus of the deep tissue. Key point: Control conditions capable of separating relief of passive constraint from postoperative rehabilitation and attention effects must be established; at the same time, changes in fat pad volume must be recorded to distinguish the independent contributions of relief of sclerotic tissue constraint and reduction of fat volume. To confirm that the intervention removed sclerotic tissue rather than simple fat, preoperative SWE and B-mode fibrosis scoring, intraoperative records of fibrous septa and investing fascia management, and collagen quantification of postoperative specimens when available should be prespecified as criteria. The primary analysis should be restricted to cases meeting these criteria.

In the intervention direction of relief of passive constraint, randomized controlled evidence already suggests that fascial stiffness itself can serve as an intervenable mechanical target. The randomized controlled trial by Ciborowski et al. (2026) showed that a phenotype-guided myofascial treatment protocol was significantly superior to the control group at 2-week follow-up (stiffness difference 2.29 kPa, 95% CI 2.12–2.45, g = 0.97) (26). Boundaries: the study population had non-specific neck pain rather than forward head posture or dorsocervical hump; the outcomes were stiffness and pain threshold rather than head position.

5.3. Tier 3: Longitudinal Cohort and Early-Versus-Late Differences

Establish a longitudinal cohort in adolescents/young adults with FHP, measure head position, deep tissue stiffness of the dorsocervical hump, fat pad thickness, and behavioral factors at baseline, and follow the cohort for several years to observe whether sclerosis forms over time and whether forward head posture becomes difficult to correct through training after sclerosis has formed. Test the prediction that early-stage FHP (before sclerosis has formed) responds well to training, whereas late-stage FHP (after sclerosis has formed) responds poorly to training (4). This tier is the key to distinguishing whether sclerosis is an initiating factor or a maintaining factor.

The correspondence among the four predictions, the three falsifiable components, and the three-tier validation pathway is as follows: Prediction 1 corresponds to the weight component and is tested cross-sectionally in Tier 1, with the refutation condition being that the independent explanatory power of sclerosis severity does not exceed the combined explanatory power of muscle and behavioral factors after controlling for fat pad thickness, muscle function, and behavioral factors; Prediction 2 corresponds to the independence component and is tested in a Tier 1 subgroup, with the refutation condition being that residual forward head posture after elimination of behavioral factors correlates with current behavior rather than with stiffness; Prediction 3 corresponds to the removal-effect component and is tested in a controlled Tier 2 study. The refutation condition is that head-position improvement after removal of sclerotic tissue is not significantly greater than that in the rehabilitation group and, where a non-sclerotic tissue comparator is included, is not significantly greater than that in the comparator group. A further refutation condition is that the improvement is unrelated to preoperative stiffness. Prediction 4 corresponds to the weight component and the independence component and is tested longitudinally in Tier 3, with refutation conditions specified separately as in Section 4: if the training effect in late-stage individuals is not significantly lower than that in early-stage individuals, the weight component is refuted, whereas the independence component still requires separate testing by Prediction 2, and only simultaneous refutation of both constitutes a joint refutation.

6. Discussion

6.1. Revision of the Existing Literature Narrative by the Hypothesis

The existing literature positions the dorsocervical hump and its deep soft tissue changes as a secondary consequence or co-localized accompanying phenomenon of FHP, with their mechanical weight regarded as lower than that of muscle imbalance and behavioral habits. This narrative may be accurate in the early stages of FHP. However, the present hypothesis proposes that in individuals with long-standing FHP, the deep sclerotic tissue of the dorsocervical hump may already have acquired relative mechanical independence, with a passive constraint weight that may exceed that of muscle and behavioral factors. This revision does not negate the main direction from forward head posture to fibrotic sclerosis, but supplements it with the reverse weight, from sclerosis to the maintenance of forward head posture, which may be non-negligible in long-standing individuals.

6.2. Clinical Implications of the Hypothesis (Requiring Strict Qualification)

If the hypothesis holds, the logic of FHP intervention may require partial adjustment: for individuals with long-standing FHP in whom deep sclerotic tissue of the dorsocervical hump has already formed, posture correction training alone may encounter a passive mechanical resistance. However, this implication must be strictly qualified: this article is a purely theoretical argument and does not constitute evidence for any specific treatment modality as a routine option for FHP; before validation in rigorously controlled studies, any intervention aimed at relieving passive constraint should not be promoted as routine management for FHP. This article does not discuss specific surgical methods or technical procedures.

6.3. Relationship Between the Hypothesis and Research on Health Consequences of FHP

The present hypothesis addresses the mechanical question of how FHP is maintained, not the causal question of whether FHP leads to specific health outcomes. If the hypothesis holds, it may provide a more precise exposure definition for the latter—that is, FHP with concurrent deep sclerotic tissue of the dorsocervical hump may be a more specific exposure dimension than FHP itself.

6.4. Limitations

Limitations on the literature side: The existing literature lacks human longitudinal evidence for the progression from chronic FHP to deep structural sclerosis of the dorsocervical hump; Liao 2023 measured the nuchal fascia rather than the deep tissue of the dorsocervical hump; Wu 2025 measured ossification rather than fibrotic sclerosis; Takeshita 2004 measured the normal nuchal ligament rather than pathological sclerotic tissue; the SWE study of post-radiation fibrosis (16) does not match in either population or etiology; Rios-Peralta 2026 was a computational simulation rather than an in vivo measurement; and the anatomical study of the nuchal ligament–spinal dura mater (18) did not involve FHP or sclerosis, and the existence of this continuity itself is subject to method-dependent controversy (19). Although the comparative histological study cited in Section 3.1 (3) confirmed that dorsocervical adipose tissue contains more prominent fibrous connective tissue, it was not specifically conducted in patients with dorsocervical hump, did not measure stiffness, and did not involve head position. Although Wang et al. (2) confirmed by cadaveric dissection and histology that the posterior cervical fat pad consists of superficial and deep layers, the sample size was limited, superficial and deep collagen density or stiffness were not directly compared, and head position was not measured; therefore, it cannot be concluded that the deep layer is fibrosis-dominant. Although Pavan et al. (5) distinguished densification from fibrosis, their work was a narrative review that did not involve the posterior cervical region or forward head posture. Chiang and Chu (14) was a narrative review with a single case report; the authors themselves described their observations as hypothesis-generating, and postural parameters and tissue stiffness were not measured; Zhou et al. (12) was a retrospective case series whose main outcomes were contour improvement and patient-reported cervical extension range of motion, without measurement of tissue stiffness or forward head angle, and it supports only the independence and operative difficulty of the fibrosis-dominant subtype, not the claim that removal of sclerotic tissue improves head position.

The mismatch between the evidence cited in this article and the target of the hypothesis can be summarized briefly. Boundary statements have already been made at first citation in each section of the main text and are not repeated in detail here.

Regarding measurement targets, Liao 2023 (8) measured the nuchal fascia in 16 healthy adults as an acute change, not deep tissue of the dorsocervical hump and not chronic sclerosis. Wu 2025 (13) measured ossification of the nuchal ligament and cephalometric parameters; ossification is not equivalent to fibrotic sclerosis. Takeshita 2004 (17) measured the normal nuchal ligament ex vivo, not pathological sclerotic tissue.

Regarding etiology and population, Dapper 2026 (16) involved post-radiation cervical fibrosis, with neither the etiology nor the population corresponding to the target, and its increased stiffness–range-of-motion dissociation has already been transformed into a boundary condition in Section 3.4. Rios-Peralta 2026 (20) was a computational simulation of normal ligaments, not in vivo and not sclerotic tissue. Ciborowski 2026 (26) involved non-specific neck pain with stiffness as the outcome, not an FHP population and not a head-position outcome.

Regarding anatomy and histology, Sillevis 2020 (18) addressed anatomical continuity between the nuchal ligament and the spinal dura mater, did not involve FHP or sclerosis, and the continuity itself is controversial (19). Sevastianova 2011 (3) addressed the histology of dorsocervical versus abdominal subcutaneous adipose tissue, was not conducted in patients with dorsocervical hump, and did not measure stiffness or head position. Wang 2022 (2) addressed the superficial/deep two-layer anatomy of the posterior cervical fat pad and did not compare superficial and deep collagen density or stiffness.

Regarding definitions and pathological classification, Pavan 2014 (5) was a review of fascial densification versus fibrosis and did not involve the posterior cervical region or FHP. Chiang and Chu 2026 (14) was a narrative review with a single case and did not measure postural parameters or tissue stiffness. Zhou 2026 (12) was a surgical case series of the fibrosis-dominant type and did not measure stiffness or forward head angle. Ding 2026 (4) was a cross-sectional pathological classification and did not measure forward head posture or involve mechanical constraint.

The above-cited literature mainly reinforces the peripheral plausibility, methodological control, or age calibration of the hypothesis and cannot independently support the core proposition that sclerosis becomes a dominant passive constraint. Reference (2) directly supports the operational premise that the posterior cervical fat pad has superficial and deep anatomical layers, but does not itself prove that the deep layer is fibrosis-dominant and therefore still cannot independently support the core proposition.

The core measurement tool used in this article—SWE—has yielded a negative result in patients with chronic neck pain that has not yet been fully explained. A 2025 study reported that the test–retest reliability of posterior cervical fascia SWE reached ICC(3,1) ≥ 0.90, but there was no significant difference in fascial stiffness between patients with chronic neck pain and low back pain and healthy controls (9). This dissociation suggests two possibilities: first, SWE has limited sensitivity for pathological sclerosis; second, sclerosis and pain may belong to different tissue dimensions. The premise presupposed by Prediction 1 in this article—that SWE can capture sclerosis variance associated with forward head posture—has not yet been directly validated in the FHP population. The tension created for the hypothesis by Dapper et al.'s increased stiffness–range-of-motion dissociation, and this article's response to it, are addressed in Section 3.4.

Several cited studies have important boundaries. Tereshenko et al. (23) did not measure the degree of fibrosis or stiffness, and the tissue source in He et al. (24) was skin rather than posterior cervical fascia. The context of Otto and Klingler (25) was tumor-associated fascial remodeling. The 2026 pathological classification study (4) was cross-sectional and did not measure forward head posture or mechanical constraint, and the population in Ciborowski et al. (26) had non-specific neck pain rather than FHP. The ultrasound-assisted liposuction study (11) was a small-sample retrospective study without stiffness or head-position measures, and the systematic review (10) used recurrence and complications as the main outcome domains. Béréziat et al. (7) involved lipodystrophy rather than typical dorsocervical hump, and Xing et al. (1) was a meta-analysis of FHP with neck pain that cannot be directly extrapolated to asymptomatic FHP. The upper trapezius SWE study (21) measured muscle rather than fascia, and the population in Blomgren et al. (22) had neck pain rather than FHP. MacFarlane et al. (6) provided only candidate mechanistic plausibility for the TGF-β/BMP pathway, not direct target-tissue evidence. Sclerosis is affected by multiple factors and should not be reduced to a single mechanical causation.

The core evidence in this article does not cite preprints, conference abstracts, or registered experiments. All literature anchored as premises consists of formally published peer-reviewed papers.

In addition, the existing surgical literature focuses on contour improvement and surgical technique selection rather than postural mechanical outcomes. The clinical validation basis for Prediction 3 (removal effect) is currently absent, rather than limited. The Prediction 1 requirement that sclerosis severity independently predict forward head posture beyond fat pad thickness, muscle function, and behavioral factors also currently has no direct empirical precedent; this is not a literature omission but rather the research gap identified by the hypothesis. The hypothesis itself is a falsifiable proposition that has not yet been validated; its value lies in proposing a research direction rather than providing clinical conclusions.

7. Conclusion

This article proposes a falsifiable mechanical hypothesis: in individuals with long-standing forward head posture, the deep sclerotic fibrous tissue of the dorsocervical hump—that is, tissue at the cervicothoracic junction in which the investing fascia has undergone fibrosis and increased stiffness—may have evolved from a secondary consequence into a dominant passive constraint and may constitute the main mechanical resistance to returning the head to a neutral position. According to the operational threshold used in this article, dominance must be tested simultaneously by a mechanical threshold criterion and a joint model criterion; the former is a necessary but not sufficient condition, and only the latter directly compares the relative explanatory power of passive constraint, muscle function, and behavioral factors. Deep sclerotic tissue is an operational designation for a mechanical functional unit and does not presuppose equal degrees of fibrosis across the three anatomical components. The hypothesis targets sclerosis (increased stiffness), not increased volume or fat accumulation. The hypothesis comprises three falsifiable components: a weight component (the contribution weight of passive constraint is greater than the combined contribution of muscle and behavioral factors), an independence component (once sclerotic tissue has formed, it acquires mechanical independence relative to the original behavioral factors), and a removal-effect component (head-position improvement after removal of sclerotic tissue is significantly greater than that in controls). This article presents four testable predictions and a three-tier validation pathway: Prediction 1 tests the weight component through cross-sectional independent explanatory power; Prediction 2 tests the independence component in a subgroup in which behavioral factors have been reduced; Prediction 3 tests the removal effect in a controlled study; and Prediction 4 tests early-versus-late differences in a longitudinal cohort, thereby comprehensively testing the weight and independence components. Before validation in rigorously controlled studies, this hypothesis should not be read as evidence for any specific treatment modality as a routine option for FHP; its value lies in highlighting that the existing literature positions the deep sclerotic tissue of the dorsocervical hump as a secondary consequence, and in suggesting that this framing may systematically underestimate its mechanical weight in long-standing FHP.

Conflicts of Interest Statement: The author declares no conflicts of interest.

Ethics Statement: This article is a theoretical hypothesis study; no human participants or animal experiments were performed. Therefore, no ethics approval was required. All cited data are derived from previously published literature.

Funding Statement: This work received no funding support.