Mandible, Vertical & Sleep Apnea

Evidence Supporting Mandibular Retrusion and Loss of Posterior Vertical Dimension as Causal Factors in Obstructive Sleep Apnea: A Review of Selected Literature

1. Introduction

1.1. Overview of Obstructive Sleep Apnea (OSA)

Obstructive Sleep Apnea (OSA) is a prevalent sleep-related breathing disorder characterized by recurrent episodes of partial (hypopnea) or complete (apnea) collapse and obstruction of the upper airway during sleep.¹ These obstructive events lead to intermittent hypoxia, hypercapnia, and frequent arousals from sleep, resulting in fragmented, nonrestorative sleep patterns.¹ Clinically, OSA often manifests with symptoms such as loud, disruptive snoring, witnessed breathing pauses, gasping or choking during sleep, and excessive daytime sleepiness.¹ The condition carries significant health implications, increasing the risk for cardiovascular diseases (including hypertension, ischemic heart disease, stroke, heart failure, and atrial fibrillation), metabolic dysfunction, neurocognitive impairments (such as deficits in memory and concentration), reduced quality of life, and increased risk of accidents.¹ The pathophysiology of OSA is understood to be complex and multifactorial, involving an interplay between anatomical factors that predispose the upper airway to narrowing and collapse, and non-anatomical factors such as impaired neuromuscular control of airway dilator muscles and ventilatory control instability.¹ A critical element in OSA development is the inherent collapsibility of the pharyngeal airway.¹² Various factors can contribute to this increased collapsibility, including obesity (particularly central fat distribution and increased neck circumference), enlargement of soft tissues within the airway (such as the tongue, soft palate, and lateral pharyngeal walls), adenotonsillar hypertrophy (especially significant in pediatric OSA), and specific craniofacial skeletal characteristics. ¹

The pathophysiology of OSA is understood to be complex and multifactorial, involving an interplay between anatomical factors that predispose the upper airway to narrowing and collapse, and non-anatomical factors such as impaired neuromuscular control of airway dilator muscles and ventilatory control instability.¹ A critical element in OSA development is the inherent collapsibility of the pharyngeal airway.¹² Various factors can contribute to this increased collapsibility, including obesity (particularly central fat distribution and increased neck circumference), enlargement of soft tissues within the airway (such as the tongue, soft palate, and lateral pharyngeal walls), adenotonsillar hypertrophy (especially significant in pediatric OSA), and specific craniofacial skeletal characteristics.¹

1.2. Report Focus and Scope

This report aims to critically evaluate and synthesize the evidence available within a defined set of literature sources that specifically supports the hypothesis that two anatomical factors – mandibular retrusion (retrognathia) and loss of posterior vertical dimension of occlusion (VDO) – act as causal contributors to the etiology or severity of Obstructive Sleep Apnea. While acknowledging the established multifactorial nature of OSA ⁷, the primary objective here is to isolate and analyze the arguments and data presented in the provided materials ² that point towards a causal role for these specific craniofacial and dental features. The scope of this review is therefore strictly limited to the information contained within these designated sources, focusing on building the case for causality as pertains to mandibular retrusion and VDO loss in the context of OSA pathogenesis.

2. Mandibular Retrusion as an Etiological Factor in OSA

2.1. Defining Mandibular Retrusion and its Relevance

Mandibular retrusion, often used interchangeably with the term retrognathia, describes a condition where the mandible (lower jaw) is positioned more posteriorly than its ideal or normal location relative to the maxilla (upper jaw) or the cranial base when viewed from a lateral perspective.¹ This skeletal discrepancy often manifests clinically as a Class II malocclusion, where the mandibular teeth are positioned posterior to their normal relationship with the maxillary teeth.⁷ Retrognathia implies a deficiency in the anteroposterior (AP) growth or position of the mandible.¹⁶

Assessment of mandibular position is commonly performed using lateral cephalometric radiography, a standardized X-ray of the side of the head. Cephalometric analysis involves measuring various angles and distances between specific anatomical landmarks on the skull and jaws.¹³ A key measurement used to quantify mandibular retrusion is the SNB angle (Sella-Nasion-B point), which relates the anteroposterior position of the mandible (point B) to the cranial base (Sella-Nasion line). A smaller SNB angle compared to population norms (e.g., an SNB of 72 degrees versus a norm of ~80 degrees) is indicative of mandibular retrusion.¹⁶ Another relevant measure is the ANB angle (A point-Nasion-B point), which reflects the sagittal relationship between the maxilla and mandible; an increased ANB angle often suggests mandibular retrusion relative to the maxilla.² Clinical examination can also provide clues, such as an exaggerated convex facial profile or a reduced thyromental distance (the distance from the thyroid cartilage to the chin).¹ Mandibular retrusion is recognized as an anatomical risk factor for OSA ¹, and its presence is often noted during the physical examination of OSA patients.¹

2.2. Anatomical Rationale: How Retrusion Contributes to Airway Narrowing

The causal link between mandibular retrusion and OSA is primarily based on the direct anatomical consequences of a posteriorly positioned mandible on upper airway dimensions. The tongue, particularly its base, is attached to the inner aspect of the mandible (via the genioglossus muscle attaching to the genial tubercles). When the mandible is retruded, it inherently displaces the tongue base posteriorly.⁷ This posterior displacement encroaches upon the pharyngeal airway space, particularly the retrolingual region (the area behind the tongue base) and potentially the retropalatal region (behind the soft palate).⁷

This anatomically narrowed airway is inherently more susceptible to collapse, especially during sleep when there is a physiological reduction in the activity and tone of upper airway dilator muscles, including the genioglossus.¹ The combination of a structurally smaller airway due to mandibular retrusion and the functional changes during sleep creates a condition where the negative pressure generated during inspiration can more easily overcome the airway's structural integrity, leading to partial or complete obstruction.¹ Therefore, mandibular retrusion initiates a chain of events: the retruded skeletal framework leads to posterior tongue displacement, which causes a reduction in the posterior airway space dimension, thereby increasing the physical susceptibility of the airway to collapse (pharyngeal collapsibility) during the hypotonic state of sleep, ultimately manifesting as OSA.¹ The increased pressure from surrounding soft tissues onto a smaller bony enclosure may further contribute to this collapsibility.¹

2.3. Evidence from Cephalometric Studies

Numerous studies utilizing cephalometric analysis have provided quantitative evidence supporting the association between specific mandibular characteristics and OSA. By comparing measurements in individuals with OSA to those in control groups without OSA, researchers have identified consistent patterns suggesting that mandibular morphology plays a significant role in the condition.

Key findings frequently reported in OSA patients include:

• Shorter Mandibular Length: Several studies have documented that individuals with OSA tend to have mandibles that are shorter in overall length (e.g., measured from Gonion to Gnathion or using other standardized points) compared to non-OSA controls.² One study specifically found that mandibular length and depth were significantly smaller in men with OSA, and calculated that a one standard deviation increase in mandibular length or depth was associated with an approximately halved risk of OSA in men (Odds Ratio ≈ 0.5), suggesting a protective effect of larger mandibular dimensions.⁸ Another recent study confirmed significantly shorter mandibular lengths in OSAS patients compared to controls.²

• Mandibular Retrognathia/Retrusion: Studies often report findings indicative of a more posteriorly positioned mandible in OSA cohorts. This is reflected in measurements such as a reduced SNB angle ¹⁹ or an increased ANB angle (indicating greater sagittal skeletal jaw discrepancy).² One systematic review focusing on pediatric OSA found that affected children tended to have mandibular retroposition or retrognathia, evidenced by a significantly greater ANB angle compared to controls.²⁰ Another review also identified a subgroup of pediatric OSA patients with increased mandibular retrognathia (reduced SNB).¹⁹ While one study reported retrognathia in only 24% of its adult OSA sample ¹⁸, others found features like a "receding mandible" to be characteristic.¹⁷

• Inferior Hyoid Bone Position: The hyoid bone, a U-shaped bone in the neck that supports the tongue, is frequently found to be positioned more inferiorly (lower down in the neck) and sometimes more posteriorly in OSA patients relative to cranial or mandibular landmarks.² This altered hyoid position is significant because it impacts tongue posture and the shape of the hypopharyngeal airway.⁸ An inferiorly positioned hyoid may reflect adaptation to a crowded airway or contribute to airway narrowing itself. One study found that the distance between the hyoid bone and the mandibular plane (MP-H) was significantly longer in severe OSA patients and could serve as a predictor for OSA severity.²³ Another investigation suggested that the inferior hyoid position observed in apneics might be associated with enlarged tongue volume.⁸

• Reduced Posterior Airway Space (PAS): Direct measurement of the airway space on cephalograms often reveals a narrower PAS (the space behind the base of the tongue) in OSA patients.¹⁷

The consistency of these quantitative differences across multiple studies strongly suggests that these craniofacial features, particularly a smaller and/or more retruded mandible, are not merely incidental findings but represent a structural predisposition to airway collapse. The altered mandibular morphology physically limits the space available for the tongue and other soft tissues, directly impacting airway dimensions. The associated finding of an inferiorly positioned hyoid bone further supports this structural link, as the hyoid's position is intimately related to both mandibular position and the posture of the tongue base and epiglottis, critical structures for maintaining airway patency.

Table 1: Cephalometric Indicators of Mandibular Position and Facial Height Associated with OSA

2.4. Evidence from Intervention Studies (Mandibular Advancement)

Further compelling evidence for the causal role of mandibular retrusion comes from intervention studies where the position of the mandible is intentionally altered. If a retruded mandible contributes to OSA, then advancing it should alleviate the condition. This is precisely what is observed with treatments like mandibular advancement surgery and Mandibular Advancement Devices (MADs).

• Surgical Advancement: Case reports and studies have documented the successful resolution or significant improvement of OSA following surgical procedures that advance the mandible (orthognathic surgery), particularly in patients who presented with mandibular retrusion pre-operatively.⁶ One case study detailed a non-obese patient with documented OSA and mandibular retrusion whose OSA resolved completely after surgical mandibular advancement combined with orthodontic and prosthetic rehabilitation, without any surgery on the palate.⁶ Maxillomandibular advancement (MMA) surgery, which advances both jaws, is noted to be particularly effective in patients with retrognathia.¹

• Mandibular Advancement Devices (MADs): MADs are oral appliances worn during sleep that hold the mandible in a protruded position.⁵ They are a wellestablished treatment for mild to moderate OSA and an alternative for some severe cases.⁴ The mechanism of action is primarily attributed to the physical advancement of the mandible, which pulls the tongue forward and increases the dimensions of the pharyngeal airway, reducing its collapsibility.⁵ Numerous studies confirm the efficacy of MADs in reducing the Apnea-Hypopnea Index (AHI), improving oxygen saturation, reducing snoring, and alleviating daytime sleepiness.⁴ The widespread success of MAD therapy provides strong, albeit indirect, evidence that the baseline mandibular position (often relatively retruded, even if not severely retrognathic) is a key factor in airway obstruction for many OSA patients. Some research suggests that MADs should be designed considering individual mandibular morphology to prevent unintentional mandibular retrusion during mouth opening, further implying that mandibular position is critical.²⁵ Cephalometric studies have also been used to predict airway response to mandibular protrusion with MADs, linking features like a normal anteroposterior jaw relationship to a better outcome.³⁰

The consistent therapeutic benefit derived from physically moving the mandible forward —whether temporarily with an appliance or permanently through surgery—strongly supports the contention that the initial, more retruded position was a contributing cause of the airway obstruction. If mandibular position were merely correlated with OSA without a causal link, interventions specifically targeting and altering this position would not be expected to yield such consistent improvements in airway patency and clinical outcomes. The effectiveness of these advancement therapies serves as a functional confirmation of the anatomical principles linking mandibular position to airway size and stability.

2.5. Synthesis and Caveats from Reviews

Systematic reviews and meta-analyses included in the provided literature generally support an association between mandibular retrusion or related craniofacial features and OSA. For instance, reviews focusing on pediatric OSA concluded that affected children often exhibit mandibular retroposition or retrognathia and increased sagittal jaw discrepancies.¹⁹

However, it is important to acknowledge certain caveats and limitations noted within these sources:

• Not all individuals with mandibular retrusion develop OSA. One early study investigated 12 patients with Class II malocclusion (indicative of retrusion) who required mandibular advancement surgery but had no sleep complaints. Overnight polysomnography confirmed that none of these individuals had OSA, leading the authors to conclude that the incidence of OSA in this specific asymptomatic surgical population was likely no more than 26.5%.¹⁴ This suggests that mandibular retrusion alone may not be sufficient to cause OSA in the absence of other contributing factors.

• Some systematic reviews, while finding associations, express caution regarding the strength of evidence for a direct causal link, often citing heterogeneity among included studies, potential methodological limitations, or findings where the average difference between OSA and control groups, while statistically significant, might be small in clinical terms.¹⁹ One review on pediatric OSA concluded that due to low to moderate certainty of the evidence available at the time, a clear causal relationship between craniofacial morphology and pediatric OSA could not be definitively supported, although specific malocclusion phenotypes were frequent comorbidities.¹⁹

• OSA is consistently described as a multifactorial disorder.⁷ Mandibular morphology represents just one component of a complex interplay of anatomical, neuromuscular, and physiological factors contributing to airway collapse.¹¹

Despite these important qualifications, the convergence of evidence from anatomical rationale, consistent cephalometric findings demonstrating specific mandibular differences in OSA patients, and the documented success of interventions that directly address mandibular position provides substantial support for mandibular retrusion being a significant etiological factor contributing to the pathophysiology of OSA, aligning with the focus of this report.

3. Loss of Posterior Vertical Dimension as an Etiological Factor in OSA

3.1. Defining Loss of Vertical Dimension and its Relevance

The Vertical Dimension of Occlusion (VDO) refers to the vertical distance between the upper and lower jaws when the teeth are in maximum intercuspation (i.e., fully bitten together). Loss of VDO signifies a reduction in this distance, typically occurring due to the loss of posterior teeth, severe attrition (wear) of the occlusal surfaces of teeth, or complete edentulism (loss of all teeth).³ Posterior teeth, particularly molars and premolars, are primarily responsible for maintaining the VDO. Their loss removes the "stops" that prevent the mandible from closing further. This results in a decrease in the lower facial height and alters the resting posture and potential range of motion of the mandible.³

The concept of posterior occlusal support (POS) is closely related. POS refers to the presence of occluding pairs of natural teeth in the posterior segments (premolars and molars).³¹ A lack of POS, as defined by classification systems like the Eichner index, indicates a compromised ability to maintain VDO and occlusal stability.³² Loss of POS is therefore often concurrent with, or leads to, a reduction in VDO.³¹ Edentulism represents the complete loss of VDO maintenance by natural teeth.³ This loss of vertical support is hypothesized to contribute to OSA pathogenesis through its effects on craniofacial anatomy and airway dimensions.³

3.2. Anatomical Consequences of Reduced VDO

The reduction or loss of VDO triggers a cascade of anatomical and functional changes in the orofacial region that can compromise upper airway patency:

• Altered Mandibular Position and Posture: With the loss of posterior tooth support, the mandible tends to autorotate upward and forward, leading to a decrease in lower facial height.⁹ This altered position can also affect the resting posture of the mandible during wakefulness and sleep, potentially leading to a more retruded position of the tongue base relative to the posterior pharyngeal wall.³ Edentulism specifically is associated with retraction of the tongue at rest.⁹

• Changes in Hyoid Bone Position: The altered mandibular posture resulting from VDO loss can influence the position of the hyoid bone, potentially causing it to shift.³ As the hyoid bone anchors muscles of the tongue and pharynx, its positional change can impact airway shape and stability.

• Reduced Posterior Facial Height: Loss of VDO contributes directly to a reduction in posterior facial height, a feature observed cephalometrically in some OSA patient groups.² This skeletal alteration can affect the overall balance of the craniofacial complex and potentially influence airway dimensions.

• Impaired Oropharyngeal Muscle Function: Edentulism and the associated loss of VDO can lead to impaired function and reduced tone of the oropharyngeal musculature, including the soft palate and pharyngeal muscles.³ The lack of stable occlusal support may alter neuromuscular feedback loops and muscle activity patterns.

Collectively, these morphological and functional changes—altered mandibular posture, posterior tongue displacement, potential hyoid bone repositioning, reduced facial height, and altered muscle function—can lead to a net reduction in the dimensions and stability of the pharyngeal airway space, particularly during sleep when muscle tone naturally decreases.³ This creates an anatomical environment where the airway is more prone to collapse, thus contributing to the development or worsening of OSA. The loss of posterior occlusal support fundamentally alters the structural framework supporting the airway, influencing tongue space, hyoid position, and muscle function, thereby increasing susceptibility to obstruction.³

3.3. Evidence from Studies on Edentulism and Tooth Loss

Several lines of evidence link the loss of teeth, and by implication the loss of VDO, to an increased risk or severity of OSA:

• Association with Edentulism: Studies have reported associations between complete edentulism and OSA.³ One study specifically noted a strong association between edentulism and moderate-to-severe OSA (AHI ≥15), with an odds ratio of 6.29.⁹ Another found that edentulous individuals had a higher mean AHI when sleeping without their dentures (which restore some VDO) compared to when sleeping with them.⁹ While the relationship is complex and not fully elucidated ³, these findings suggest that the anatomical changes accompanying tooth loss contribute to OSA.

• Dose-Response Relationship with Tooth Loss: A large population-based study (NHANES 2005–2008) provided compelling evidence for a graded relationship between the number of lost teeth and the risk of having signs and symptoms indicative of OSA.⁹ The study found that after adjusting for confounders like age, BMI, and sex, the prevalence of being at high-risk for OSA increased by 2% for each additional tooth lost in adults aged 25-64. Compared to individuals with minimal tooth loss (0-4 teeth), the adjusted prevalence of high-risk OSA was significantly higher in those missing 5-8 teeth (25% higher), those missing 9-31 teeth (36% higher), and those who were edentulous (61% higher).⁹ This dose-response pattern —where increasing exposure (more teeth lost) corresponds to increasing risk— strengthens the argument for a causal link, suggesting a direct, graduated impact of losing occlusal support and VDO on airway stability. It makes it less likely that the association is solely due to confounding factors often linked to both tooth loss and OSA, such as age or general health status.

• Role of Posterior Occlusal Contacts: The same NHANES study also found that, among dentate individuals, a higher number of posterior occlusal contacts was significantly protective against being at high-risk for OSA, even after adjusting for the total number of teeth lost.⁹ This finding specifically points to the importance of posterior support in maintaining airway integrity, likely through its role in preserving VDO and mandibular stability.

Table 2: Evidence Linking Tooth Loss, Edentulism, and Vertical Dimension to OSA

3.4. Evidence from Interventions Restoring Vertical Dimension

Further support for the causal role of VDO loss comes from studies examining the effects of restoring vertical dimension, primarily through the use of complete dentures in edentulous individuals.

• Effect of Denture Wear: Several sources indicate that wearing complete dentures during sleep, which restores a functional VDO, can lead to improvements in OSA parameters compared to sleeping without dentures. It is suggested that denture wear induces modifications in the position of the tongue and mandible, and enlarges the pharyngeal airway space, potentially reducing apnea episodes.³ Cephalometric studies have confirmed that wearing dentures fabricated at an acceptable VDO significantly increases the retropharyngeal space compared to the edentulous state without dentures.³

• Effect of Increasing VDO: One particularly relevant study cited used custom acrylic jigs to experimentally increase the VDO by 2 mm beyond the conventionally accepted level in edentulous subjects wearing complete dentures. Cephalometric analysis showed that this increase in VDO resulted in an even more significant enlargement of the retropharyngeal space compared to wearing dentures at the standard VDO.³ This finding strongly suggests that the vertical dimension itself plays a direct role in modulating pharyngeal airway size.

This evidence demonstrates a degree of reversibility. If the loss of VDO contributes to airway compromise, then restoring VDO via dentures should logically mitigate this effect, which appears to be the case.³ The observation that increasing the VDO can provide further airway benefit ³ reinforces the idea that vertical dimension is an important variable in airway management for these patients.

It is worth noting a point of complexity regarding VDO manipulation in the context of MAD therapy for dentate patients. Increasing the vertical opening with an appliance inherently causes the mandible to rotate posteriorly, which can place it in a more retrusive position and potentially reduce the maximum achievable protrusion.³ Some researchers have theorized that increasing VDO excessively with a MAD might negate the benefits of protrusion by decreasing the space between the tongue base and the posterior pharyngeal wall.³ However, studies comparing MADs with different vertical openings have yielded mixed results, with one finding similar efficacy (AHI reduction) regardless of the vertical opening, suggesting that the degree of mandibular advancement might be the more critical factor in that specific treatment context.²⁸ This complexity highlights the interplay between vertical and sagittal dimensions but does not diminish the evidence suggesting that the fundamental loss of VDO in edentulous or severely compromised dentitions contributes to OSA pathogenesis.

3.5. Link to Posterior Facial Height

The clinical concept of VDO loss finds a potential correlate in cephalometric measurements of facial height. Studies comparing OSA patients to controls have reported significantly reduced posterior facial height (PFH), typically measured as the distance from Sella (S) to Gonion (Go), in the OSA groups.² While reduced PFH can be an intrinsic skeletal pattern, it can also be a consequence of significant VDO loss over time due to posterior tooth wear or loss. Regardless of its origin, a reduced PFH implies an altered craniofacial balance and mandibular posture that may contribute to a smaller pharyngeal airway space or increased collapsibility, consistent with the mechanisms proposed for VDO loss. This cephalometric finding provides a measurable skeletal characteristic potentially linked to the functional problem of lost vertical dimension in the context of OSA.

4. Combined Influence and Evidence Synthesis

4.1. Potential Synergistic Effects

While the evidence presented supports independent roles for both mandibular retrusion and loss of posterior VDO in contributing to OSA, it is highly plausible that these factors interact synergistically to worsen airway compromise. The anatomical relationship between sagittal mandibular position and vertical dimension suggests an inherent interdependence.

Consider a patient with pre-existing mandibular retrusion. The baseline posterior airway space is already likely reduced due to the posteriorly positioned tongue base. If this individual then experiences significant posterior tooth loss leading to a reduction in VDO, the resulting upward and potentially further posterior rotation of the mandible could exacerbate the initial sagittal deficiency, further displacing the tongue posteriorly and critically narrowing the airway.

Conversely, attempts to manage OSA by altering one dimension can impact the other. As demonstrated in studies examining MADs, increasing the vertical opening causes a posterior rotation of the mandible, effectively increasing its retrusion relative to the maxilla and reducing the forward advancement achievable at the incisors.⁵ This mechanical linkage implies that the optimal mandibular position for airway patency involves a delicate balance between vertical opening and sagittal advancement. An excessive increase in VDO without sufficient compensatory protrusion could potentially worsen airway dimensions, particularly at the level of the tongue base.³

Therefore, the vertical dimension (influenced by VDO and posterior facial height) and the sagittal dimension (mandibular protrusion/retrusion) are not isolated variables but are mechanically coupled. Changes in VDO inevitably influence the effective sagittal position of the mandible and tongue base relative to the pharynx. This interplay suggests that their combined negative impact on airway patency in individuals exhibiting both mandibular retrusion and significant VDO loss is likely greater than the simple sum of their individual effects, creating a particularly high-risk anatomical substrate for OSA.

4.2. Synthesis of Evidence Supporting Causality

The literature reviewed provides multiple converging lines of evidence that support the assertion that mandibular retrusion and loss of posterior vertical dimension are causal factors in the pathophysiology of OSA:

1. Anatomical Plausibility: Clear, biomechanically sound mechanisms explain how each factor can lead to airway narrowing. Mandibular retrusion directly reduces the space available for the tongue, displacing it posteriorly.¹ Loss of VDO alters mandibular posture, potentially affecting tongue and hyoid position, reducing posterior facial height, and impairing muscle function, collectively compromising airway stability.³

2. Consistent Morphological Differences: Observational studies using cephalometry repeatedly identify statistically significant differences in mandibular size, position, and facial height between individuals with OSA and control subjects. OSA patients frequently exhibit shorter, more retruded mandibles and reduced posterior facial height.²

3. Risk Association and Dose-Response: Epidemiological and clinical data demonstrate an increased risk of OSA associated with these anatomical features. Smaller mandibular dimensions (length and depth) have been linked to increased OSA risk, particularly in men.⁸ Furthermore, population studies show a significant, dose-dependent relationship between the number of teeth lost (a proxy for VDO loss) and the prevalence of OSA signs and symptoms, strengthening the causal inference.⁹

4. Intervention Effectiveness (Reversibility): Treatments that specifically target and counteract these anatomical deficits often lead to significant improvement or resolution of OSA. Mandibular advancement, either surgically or with MADs, directly addresses retrusion and is a proven therapy.¹ Similarly, restoring VDO with dentures in edentulous individuals has been shown to improve airway dimensions and reduce AHI.³ The success of these targeted interventions provides strong functional evidence supporting the causal role of the baseline anatomical conditions they aim to correct.

Taken together, this combination of plausible biological mechanisms, consistent observational data identifying specific anatomical correlates, evidence of increased risk associated with these features (including dose-response relationships), and positive clinical outcomes following interventions that reverse these anatomical characteristics provides a robust body of evidence, based on the reviewed sources, supporting the role of mandibular retrusion and loss of posterior vertical dimension as significant causal contributors to OSA.

4.3. Acknowledging the Multifactorial Context

While this report has focused specifically on the evidence supporting mandibular retrusion and VDO loss as causal factors, it is crucial to reiterate that OSA is universally recognized as a complex and multifactorial disorder.¹ The anatomical factors discussed herein represent only part of the overall picture.

Numerous other factors contribute significantly to OSA risk and severity, as highlighted in the reviewed literature. These include:

• Obesity and Fat Deposition: Excess body weight, particularly central adiposity and fat deposition within the neck and around the pharyngeal airway structures (e.g., lateral pharyngeal walls, tongue), is a primary risk factor.¹ Increased tissue mass narrows the airway lumen and increases its collapsibility. Waist circumference has been correlated with pharyngeal critical closing pressure (Pcrit), a measure of collapsibility.¹²

• Soft Tissue Enlargement: Enlargement of structures like the tongue (macroglossia), soft palate, and tonsils/adenoids reduces airway space.¹ Tongue volume, in particular, has been linked to OSA risk and hyoid bone position.⁸ Adenotonsillar hypertrophy is a major cause of OSA in children.¹

• Neuromuscular Factors: Impaired function or coordination of the upper airway dilator muscles during sleep contributes to collapse.¹ Sleep itself causes a natural reduction in muscle tone.

• Other Factors: Advanced age, male gender, supine sleeping position, alcohol consumption, use of sedatives, smoking, and potentially genetic predisposition also influence OSA risk.¹

It is most likely that these various factors interact. For example, the effect of a retruded mandible might be amplified in the presence of obesity or a large tongue. Conversely, significant VDO loss might have a greater impact in someone with already compromised neuromuscular control. Understanding OSA requires considering the interplay between the baseline anatomical framework (including mandibular position and VDO) and these other dynamic and soft-tissue factors.

5. Conclusion

5.1. Summary of Findings

Based on the critical analysis of the provided literature, substantial evidence supports the assertion that both mandibular retrusion and the loss of posterior vertical dimension of occlusion are significant causal factors contributing to the pathophysiology of Obstructive Sleep Apnea. The convergence of multiple lines of evidence underpins this conclusion. Anatomical rationale clearly demonstrates how a posteriorly positioned mandible restricts space for the tongue base, and how loss of vertical support alters mandibular posture and oropharyngeal structures, both leading to a narrower, more collapsible airway. Comparative cephalometric studies consistently reveal measurable differences in mandibular size, position, and facial height between OSA patients and controls, identifying a common structural phenotype associated with the condition. Furthermore, risk analyses show significant associations, including a dose-response relationship between tooth loss and OSA risk, strengthening the case for causality beyond mere correlation. Perhaps most compellingly, interventions specifically designed to counteract these anatomical deficits—mandibular advancement therapies and the restoration of vertical dimension in edentulous patients—demonstrate efficacy in improving airway patency and reducing OSA severity, providing functional confirmation of the causal role of the baseline anatomical state.

5.2. Implications

The understanding that mandibular retrusion and VDO loss are causal contributors to OSA has important clinical implications. It underscores the necessity for healthcare professionals, particularly dentists, orthodontists, and sleep physicians, to carefully evaluate craniofacial and occlusal anatomy during the assessment of patients at risk for or diagnosed with OSA. Identifying features like mandibular retrognathia or significant posterior tooth loss/wear should raise suspicion for OSA and prompt appropriate screening or referral. This causal understanding provides a strong rationale for treatments that modify these anatomical factors, such as the use of Mandibular Advancement Devices (MADs), orthognathic surgery (mandibular advancement), or combined approaches. For patients with significant tooth loss or edentulism, the potential role of prosthodontic rehabilitation in restoring VDO and potentially improving airway stability should be considered as part of a comprehensive OSA management strategy, possibly in conjunction with other therapies.

5.3. Final Caveat

While the reviewed evidence strongly supports a causal role for mandibular retrusion and VDO loss in OSA, it is essential to acknowledge the multifactorial nature of the disorder. These anatomical factors interact with other elements like obesity, soft tissue volume, and neuromuscular control. Furthermore, some sources reviewed urge caution regarding the definitive establishment of causality based solely on existing observational data, citing study limitations and heterogeneity.19 Additionally, the presence of these anatomical features does not invariably lead to OSA, as demonstrated by studies on asymptomatic individuals with Class II malocclusion.14 Nonetheless, within the scope of the literature examined, the weight of evidence clearly implicates mandibular retrusion and loss of posterior vertical dimension as important and modifiable factors in the causal pathway of Obstructive Sleep Apnea for a significant portion of affected individuals.

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