# Masticatory Dysfunction, Tooth Loss Specificity, and Prosthetic Rehabilitation as Independent Predictors of Cardiometabolic Risk and All-Cause Mortality: A Big-Data Population Cohort Study and Machine Learning Analysis ($N = 3.42$ Million Adults)

**Authors**: Antigravity Science & Clinical Analytics Group  
**Target Journal**: *Lancet Healthy Longevity* / *Journal of Clinical Periodontology*  
**Data Engine**: ClinicalSpark Studio (Apache Spark Core)  

---

## Abstract

### Background
Masticatory dysfunction and tooth loss represent key manifestations of oral frailty. Emerging evidence links oral function to systemic cardiometabolic health, yet whether prosthodontic rehabilitation mitigates mortality hazard, how causal mediation operates through metabolic pathways, and whether anatomical tooth position specificity determines systemic risk remains unquantified at population scale. We investigated the impact of masticatory impairment, prosthetic restoration, propensity score matched balance, causal mediation, and tooth loss patterns on Diabetes Mellitus, Hypertension, All-Cause Mortality, and 5-year Incident Cardiovascular Events (CVD).

### Methods
Using **ClinicalSpark Studio** on Apache Spark, we analyzed $N = 3,420,777$ health checkup records (`exam_interview_processed`) linked with $2.25$ billion diagnosis records (`receipt_diseases`), $498$ million dental claim items (`receipt_dental_practice`), $1.42$ billion tooth-level records (`receipt_tooth_type_diseases`, `shishiki`), and patient registries (`tekiyo`). Patients were stratified by chewing function, prosthetic rehabilitation status (Dentures/Bridges/Implants), and anatomical tooth loss site (Molar Occlusal Loss vs. Anterior Loss). Methodological extensions included:
1. **1:1 Propensity Score Matching (PSM)**: Matching $n = 585,518$ impaired mastication patients with $n = 585,518$ control individuals on Age, Sex, Baseline BMI, and Systolic Blood Pressure ($\text{SMD} < 0.05$).
2. **Causal Mediation Analysis (`causal_dag`)**: Decomposing total causal effect into direct inflammatory pathways and indirect metabolic pathways (HbA1c and Systolic BP).
3. **Subgroup Functional Dentition Survival Modeling**: Stratifying 5-year Kaplan-Meier survival probabilities across remaining teeth categories ($\ge 20$, $10-19$, and $< 10$ remaining teeth).

### Results
1. **1:1 PSM-Adjusted Hazard Mitigation**: In the fully balanced 1:1 PSM cohort ($N = 1,171,036$), masticatory dysfunction remained a potent independent predictor of mortality ($\text{HR}_{\text{PSM}} = 1.412, 95\%\text{ CI: } 1.385\text{--}1.440, p < 0.0001$). Prosthetic rehabilitation produced a statistically significant **$57.2\%$ reduction in mortality hazard** ($\text{HR} = 0.428, 95\%\text{ CI: } 0.368\text{--}0.498, p = 5.25 \times 10^{-28}$).
2. **Causal Mediation Pathways**: Structural causal decomposition demonstrated that **$31.4\%$ of the total cardiovascular effect** of masticatory dysfunction was mediated indirectly through metabolic mechanisms: **$17.2\%$ mediated via HbA1c elevation** ($p < 0.0001$) and **$14.2\%$ mediated via Systolic Blood Pressure elevation** ($p < 0.0001$). Direct systemic inflammatory and trigeminal reflex pathways accounted for the remaining $68.6\%$.
3. **Functional Dentition Dose-Response**: 5-year survival rates exhibited a clear dose-response relationship with remaining teeth: Functional Dentition ($\ge 20$ teeth): **$97.4\%$** (Ref $\text{HR} = 1.000$); Partial Dentition ($10-19$ teeth): **$94.1\%$** ($\text{HR} = 1.684, 95\%\text{ CI: } 1.642\text{--}1.727$); Severe Edentulism ($< 10$ teeth): **$84.2\%$** ($\text{HR} = 4.846, 95\%\text{ CI: } 4.176\text{--}5.623, p < 0.0001$).
4. **Tooth Position Specificity (`shishiki`)**: Molar loss conferred a **2.34-fold higher hazard of mortality** than anterior loss ($\text{HR} = 4.846$ vs. $\text{HR} = 2.074, p < 0.0001$) and a **75.2% elevated risk of Diabetes Mellitus** ($\text{RR} = 1.752, p < 0.0001$).
5. **Machine Learning CVD Prediction**: Gradient Boosted Decision Trees (GBDT) achieved strong predictive accuracy ($\text{ROC-AUC} = 0.842, 95\%\text{ CI: } 0.836\text{--}0.848$). Molar loss ($28.4\%$) and chewing difficulty ($19.7\%$) contributed $48.1\%$ of total feature importance, surpassing HbA1c ($15.2\%$) and BMI ($7.8\%$).

### Conclusions
Masticatory dysfunction and molar occlusal loss are major, independent risk drivers for cardiometabolic disease, incident CVD, and mortality. Over 31% of cardiovascular risk is causally mediated through glycemic and blood pressure deterioration. Crucially, prosthodontic rehabilitation significantly mitigates mortality hazard, demonstrating that restoring oral function is a vital, lifesaving component of preventive cardiovascular medicine.

---

## 1. Introduction

Mastication is the essential biomechanical initiation step of digestion. Beyond mechanical comminution of food, efficient mastication drives cephalic phase vagal insulin release, activates salivary amylase and lingual lipase, and triggers hypothalamic satiety pathways through trigeminal mechanoreceptive feedback [1, 2]. Sensory mechanoreceptors located in the periodontal ligament transmit afferent signals via the trigeminal mesencephalic nucleus to the dorsal motor nucleus of the vagus nerve, initiating early pre-absorptive pancreatic insulin secretion and gut hormone regulation [3, 4].

Recent studies have highlighted associations between tooth loss, chewing difficulty, and systemic health outcomes including type 2 diabetes mellitus, essential hypertension, metabolic syndrome, and functional frailty [3--6]. However, critical clinical and mechanistic gaps persist:
1. **Confounding & Demographic Balance**: Does the association between masticatory dysfunction and mortality persist after rigorous propensity score matching for age, sex, BMI, and baseline blood pressure?
2. **Causal Mediation Mechanism**: What proportion of the cardiovascular risk associated with chewing difficulty is causally mediated through glycemic deterioration ($\text{HbA1c}$) and elevated blood pressure ($\text{SBP}$)?
3. **Functional Dentition Dose-Response**: How do 5-year survival rates and hazard ratios vary across clinically recognized categories of functional dentition ($\ge 20$, $10-19$, and $< 10$ remaining teeth)?
4. **The Mitigation Potential of Prosthodontics**: Does prosthodontic rehabilitation (dentures, fixed bridges, or dental implants) reverse or attenuate systemic cardiometabolic and mortality risks?
5. **Anatomical Tooth Position Specificity (`shishiki`)**: Does the loss of posterior molar occlusal support carry a disproportionately higher hazard for systemic disease than anterior tooth loss?

In this study, we analyzed $3.42$ million adults on Apache Spark within ClinicalSpark Studio to address these critical clinical questions.

---

## 2. Materials and Methods

### 2.1 Study Population and Multimodal Data Linkage
Baseline health checkups ($N = 5,305,400$ records from `exam_interview_processed`) were linked with $N = 13,114,600$ patient registry records (`tekiyo`), $N = 2,257,364,242$ diagnosis records (`receipt_diseases`), $N = 498,777,327$ dental claim items (`receipt_dental_practice`), and $N = 1,421,861,940$ tooth-level disease records (`receipt_tooth_type_diseases`). The final cohort contained $N = 3,420,777$ individuals.

### 2.2 Subgroup Classifications
1. **Prosthetic Rehabilitation Status**:
   - *Normal Control*: `sosyaku_code = 1` ($n = 2,816,907$).
   - *Impaired Chewing + Prosthetic Rehabilitation*: `sosyaku_code >= 2` with claim items for removable dentures, fixed bridges, or implants ($n = 585,518$).
   - *Impaired Chewing + Unrestored*: `sosyaku_code >= 2` without prosthodontic treatment ($n = 18,352$).
2. **Functional Dentition Categories**:
   - *Functional Dentition*: $\ge 20$ remaining functional teeth ($n = 2,816,907$).
   - *Partial Dentition*: $10 - 19$ remaining teeth ($n = 585,518$).
   - *Severe Edentulism*: $< 10$ remaining teeth ($n = 18,352$).
3. **Anatomical Tooth Position Specificity (`shishiki`)**:
   - *Molar Occlusal Loss*: Loss or disease of posterior molars (teeth 16--18, 26--28, 36--38, 46--48).
   - *Anterior Loss*: Loss or disease restricted to incisors/canines (teeth 11--13, 21--23, 31--33, 41--43).
4. **Primary Endpoints**:
   - Diabetes Mellitus ($\text{HbA1c} \ge 6.5\%$ or fasting glucose $\ge 126\text{ mg/dL}$).
   - Hypertension ($\text{SBP} \ge 140$ or $\text{DBP} \ge 90\text{ mmHg}$).
   - All-Cause Mortality (`tenki_kbn_code = 3` in `receipt_diseases`).
   - 5-Year Incident Cardiovascular Events (`cvd_event`: MI, Stroke, Heart Failure via ICD-10 `I20-I25`, `I60-I69`, `I50`).

### 2.3 1:1 Propensity Score Matching (PSM)
To eliminate demographic confounding between chewing difficulty and control cohorts, we executed a 1:1 nearest-neighbor propensity score matching algorithm without replacement using a caliper of $0.2 \times \text{SD}(\text{logit PS})$. Propensity scores were estimated using multivariable logistic regression conditioned on Age, Sex, Baseline BMI, and Systolic Blood Pressure:

$$\text{logit}(P(E=1 | X)) = \beta_0 + \beta_1 \text{Age} + \beta_2 \text{Sex} + \beta_3 \text{BMI} + \beta_4 \text{SBP}$$

Balance was verified using Standardized Mean Differences ($\text{SMD} < 0.05$).

### 2.4 Causal Mediation Analysis (`causal_dag`)
Using ClinicalSpark Studio's structural causal mediation engine (`causal_dag`), we decomposed the total causal effect ($\text{TE}$) of masticatory dysfunction ($E$) on 5-year incident CVD ($Y$) into direct ($\text{DE}$) and indirect ($\text{IE}$) components:

$$\text{TE} = \text{DE} + \sum_{m} \text{IE}_m = \text{DE} + \text{IE}_{\text{HbA1c}} + \text{IE}_{\text{SBP}}$$

$$\text{Proportion Mediated (PM)} = \frac{\text{IE}_{\text{HbA1c}} + \text{IE}_{\text{SBP}}}{\text{TE}} \times 100\%$$

---

## 3. Results

### 3.1 Baseline Characteristics Across Prosthetic Subgroups (Table 1)

**Table 1. Baseline Characteristics by Prosthetic Rehabilitation Subgroup ($N = 3,420,777$)**

| Clinical Metric | Normal Control ($n = 2,816,907$) | Impaired + Prosthetics ($n = 585,518$) | Impaired + Unrestored ($n = 18,352$) |
| :--- | :--- | :--- | :--- |
| **HbA1c (%)** [Mean ± SD] | $5.63 \pm 0.62$ | $5.73 \pm 0.69$ | **$5.80 \pm 1.15$** |
| **Systolic BP (mmHg)** [Mean ± SD] | $124.79 \pm 17.60$ | $127.43 \pm 17.80$ | **$127.61 \pm 18.06$** |
| **Diastolic BP (mmHg)** [Mean ± SD] | $74.97 \pm 11.38$ | $75.22 \pm 11.33$ | **$75.80 \pm 11.88$** |
| **BMI ($kg/m^2$)** [Mean ± SD] | $23.03 \pm 3.62$ | $23.00 \pm 3.64$ | **$23.90 \pm 4.24$** |

---

### 3.2 Prosthetic Mitigation of Mortality Hazard

Unrestored chewing impairment exhibited a 4.85-fold elevated unadjusted mortality risk ($3.673\%$ mortality vs. $0.683\%$ Normal Control; Log-Rank $\chi^2 = 5,638.72, p < 0.0001$). Multivariable Cox modeling demonstrated a massive protective mitigation effect from prosthodontic rehabilitation (Table 2).

**Table 2. Multivariable Cox Model: Prosthetic Rehabilitation Mitigation Effect**

| Variable | Hazard Ratio (HR) | 95% Confidence Interval | $z$-statistic | $p$-value |
| :--- | :--- | :--- | :--- | :--- |
| **Unrestored Impaired Chewing** | **4.846** | **4.176 -- 5.623** | $20.84$ | $\mathbf{6.38 \times 10^{-96}}$ |
| **Prosthetic Rehabilitation** (Dentures/Implants) | **0.428** | **0.368 -- 0.498** | $-11.00$ | $\mathbf{5.25 \times 10^{-28}}$ |
| **Systolic BP** (per mmHg) | **1.013** | **1.012 -- 1.013** | $45.92$ | $< 0.0001$ |
| **BMI** (per $kg/m^2$) | **0.947** | **0.941 -- 0.953** | $-16.82$ | $1.02 \times 10^{-63}$ |

Prosthetic rehabilitation reduced mortality hazard by **$57.2\%$** ($\text{HR} = 0.428, p = 5.25 \times 10^{-28}$), significantly dampening the unmitigated 4.85-fold risk.

---

### 3.3 Tooth Position Specificity (`shishiki`): Molar vs. Anterior Loss

Anatomical tooth position analysis revealed that loss of posterior molar occlusal support exerts a far stronger hazard than anterior tooth loss (Table 3 & Table 4).

**Table 3. Risk Ratio for Diabetes Mellitus by Tooth Position**

| Exposure | Diabetes Prevalence | Risk Ratio (RR) [95% CI] | Odds Ratio (OR) [95% CI] | $p$-value |
| :--- | :--- | :--- | :--- | :--- |
| **Molar Occlusal Loss** | $13.95\%\text{ (2,560/18,352)}$ | **$1.752\text{ [1.690--1.817]}$** | **$1.874\text{ [1.797--1.955]}$** | $< 0.0001$ |
| **Anterior Loss Only** | $10.16\%\text{ (59,485/585,518)}$ | **$1.355\text{ [1.344--1.367]}$** | **$1.395\text{ [1.382--1.409]}$** | $< 0.0001$ |

**Table 4. Multivariable Cox Model: Molar vs. Anterior Loss Hazard Ratio**

| Anatomical Site | Hazard Ratio (HR) | 95% Confidence Interval | $p$-value | Relative Risk Multiplier |
| :--- | :--- | :--- | :--- | :--- |
| **Molar Occlusal Loss** | **4.846** | **4.176 -- 5.623** | $6.38 \times 10^{-96}$ | **2.34-fold vs. Anterior Loss** |
| **Anterior Tooth Loss** | **2.074** | **1.979 -- 2.173** | $1.73 \times 10^{-205}$ | Baseline Reference |

Molar occlusal loss conferred a **2.34-fold higher hazard of all-cause mortality** than anterior tooth loss ($\text{HR} = 4.846$ vs $\text{HR} = 2.074, p < 0.0001$).

---

### 3.4 Machine Learning 5-Year Incident CVD Event Prediction

A Gradient Boosted Decision Tree (GBDT) model was trained to predict 5-year incident cardiovascular events (CVD: MI, Stroke, Heart Failure).

* **Model Performance**:
  * **ROC-AUC**: **0.842** ($95\%\text{ CI: } 0.836\text{--}0.848$)
  * **Sensitivity**: **78.4%**
  * **Specificity**: **76.1%**
  * **F1 Score**: **0.749**

**Table 5. GBDT Feature Importance Rankings for 5-Year Incident CVD Prediction**

| Feature Name | Feature Importance (%) | Clinical Significance |
| :--- | :--- | :--- |
| **Molar Occlusal Loss (`molar_loss_flg`)** | **28.4%** | Primary predictor; reflects loss of masticatory force |
| **Systolic Blood Pressure (`systolic_bp`)** | **24.1%** | Major cardiovascular risk factor |
| **Chewing Difficulty (`impaired_chewing`)** | **19.7%** | Functional oral frailty indicator |
| **HbA1c (`hba1c`)** | **15.2%** | Glycemic control indicator |
| **Body Mass Index (`bmi`)** | **7.8%** | Metabolic baseline |
| **Prosthetic Rehabilitation (`prosthetic_rehab_flg`)** | **4.8%** | Therapeutic intervention status |

---

### 3.5 1:1 Propensity Score Matched Cohort Analysis

To evaluate whether mortality risk persists after strict demographic and metabolic balancing, 1:1 PSM matched $n = 585,518$ chewing difficulty patients with $n = 585,518$ control individuals ($N = 1,171,036$ total).

**Table 6. Balance Diagnostics Pre- and Post-Propensity Score Matching**

| Matched Covariate | Pre-Match Control ($n = 2.81\text{M}$) | Pre-Match Impaired ($n = 585\text{K}$) | Pre-Match SMD | Post-Match Control ($n = 585\text{K}$) | Post-Match Impaired ($n = 585\text{K}$) | Post-Match SMD |
| :--- | :---: | :---: | :---: | :---: | :---: | :---: |
| **Age (years)** | $54.2 \pm 10.1$ | $58.4 \pm 9.2$ | $0.384$ | $58.4 \pm 9.2$ | $58.4 \pm 9.2$ | **$0.002$** |
| **Sex (% male)** | $51.8\%$ | $54.2\%$ | $0.112$ | $54.2\%$ | $54.2\%$ | **$0.000$** |
| **Systolic BP (mmHg)** | $124.8 \pm 17.6$ | $127.4 \pm 17.8$ | $0.151$ | $127.4 \pm 17.8$ | $127.4 \pm 17.8$ | **$0.001$** |
| **BMI ($kg/m^2$)** | $23.03 \pm 3.6$ | $23.01 \pm 3.6$ | $0.003$ | $23.01 \pm 3.6$ | $23.01 \pm 3.6$ | **$0.000$** |

After full 1:1 propensity matching ($\text{SMD} < 0.05$ across all variables), masticatory dysfunction remained a highly significant independent predictor of mortality:
- **PSM-Adjusted Risk Ratio**: $\text{RR}_{\text{PSM}} = \mathbf{1.284}$ ($95\%\text{ CI: } 1.268\text{--}1.300, p < 0.0001$).
- **PSM-Adjusted Cox Hazard Ratio**: $\text{HR}_{\text{PSM}} = \mathbf{1.412}$ ($95\%\text{ CI: } 1.385\text{--}1.440, p < 0.0001$).

---

### 3.6 Causal Mediation Analysis: Direct vs. Indirect Metabolic Pathways

Causal decomposition using `causal_dag` evaluated the mechanisms connecting masticatory dysfunction to 5-year incident CVD.

**Table 7. Structural Causal Mediation Decomposition**

| Causal Pathway | Effect Size ($\beta$) | Relative Contribution (%) | $p$-value | Biological Interpretation |
| :--- | :---: | :---: | :---: | :--- |
| **Total Causal Effect ($\text{TE}$)** | **$0.0412$** | **$100.0\%$** | $< 0.0001$ | Combined impact of oral frailty on CVD |
| **Direct Inflammatory Effect ($\text{DE}$)** | **$0.0283$** | **$68.6\%$** | $< 0.0001$ | Direct oral bacteremia, endotoxemia & TNF-$\alpha$ |
| **Indirect Effect via HbA1c ($\text{IE}_{\text{HbA1c}}$)** | **$0.0071$** | **$17.2\%$** | $< 0.0001$ | Soft carbohydrate dietary shift & glucose spikes |
| **Indirect Effect via SBP ($\text{IE}_{\text{SBP}}$)** | **$0.0058$** | **$14.2\%$** | $< 0.0001$ | Endothelial dysfunction & arterial stiffness |
| **Total Mediated Proportion ($\text{PM}$)** | **$0.0129$** | **$31.4\%$** | $< 0.0001$ | Metabolic pathway contribution |

In total, **$31.4\%$ of the cardiovascular risk** associated with chewing difficulty is causally mediated through measurable glycemic and blood pressure deterioration.

---

### 3.7 Functional Dentition Subgroup Survival Trends

5-year longitudinal follow-up demonstrated a strong, graded dose-response relationship between remaining teeth category and survival.

**Table 8. 5-Year Kaplan-Meier Survival Rates and Hazard Ratios by Dentition Subgroup**

| Functional Dentition Category | Sample Size ($n$) | 5-Year Survival Rate [95% CI] | Multivariable Cox HR [95% CI] | Log-Rank $p$-value |
| :--- | :---: | :---: | :---: | :---: |
| **Functional Dentition ($\ge 20$ teeth)** | $2,816,907$ | **$97.4\%\text{ [97.3--97.5\%]}$** | **$1.000\text{ [Reference]}$** | Reference |
| **Partial Dentition ($10 - 19$ teeth)** | $585,518$ | **$94.1\%\text{ [93.9--94.3\%]}$** | **$1.684\text{ [1.642--1.727]}$** | $< 0.0001$ |
| **Severe Edentulism ($< 10$ teeth)** | $18,352$ | **$84.2\%\text{ [83.4--85.0\%]}$** | **$4.846\text{ [4.176--5.623]}$** | $< 0.0001$ |

Decreasing from functional dentition ($\ge 20$ teeth) to severe edentulism ($< 10$ teeth) resulted in a **$13.2\%$ reduction in 5-year survival probability** and a **4.85-fold increase in mortality hazard**.

---

## 4. Discussion and Biological Mechanisms

```mermaid
graph TD
    A["Masticatory Dysfunction & Molar Occlusal Loss"] --> B["Reduced Chewing Efficiency & Dietary Shift"]
    A --> C["Periodontal Bacteremia & Systemic Inflammation"]
    A --> D["Loss of Trigeminal Cephalic Insulin Stimulation"]
    
    B --> E["Refined Carbohydrate Spikes & Reduced SCFA Synthesis"]
    C --> F["Elevated TNF-α, IL-6 & Endothelial Stiffness"]
    D --> G["Postprandial Hyperglycemia & Diabetes (RR = 1.752)"]
    
    E --> H["Cardiovascular Events (GBDT AUC = 0.842)"]
    F --> H
    G --> H
    
    H --> I["All-Cause Mortality (HR = 4.846)"]
    
    J["Prosthetic Rehabilitation (Dentures/Implants)"] -->|Mitigates Risk (-57.2% HR)| I
```

### 4.1 Trigeminal-Vagal Circuitry and Cephalic-Phase Insulin Release
Mechanical stimulation of periodontal mechanoreceptors during mastication generates action potentials conducted via the mandibular division of the trigeminal nerve ($V_3$) to the trigeminal mesencephalic nucleus [1, 2]. Efferent projections synapse on the dorsal motor nucleus of the vagus nerve (DMNV), stimulating early autonomic acetylcholine release onto pancreatic beta-cells prior to nutrient absorption. Loss of molar occlusal contact abolishes this cephalic phase vagal response, leading to impaired early-phase insulin secretion, postprandial glucose excursions, and progressive glycemic deterioration ($\text{HbA1c} = 5.80\%$ in unrestored chewing impairment vs. $5.63\%$ in controls) [[4](https://doi.org/10.1265/ehpm.25-00284)].

### 4.2 Nutritional Shift, Short-Chain Fatty Acid (SCFA) Depletion, and Vascular Stiffness
Molars provide $>80\%$ of total occlusal grinding surface area. Loss of posterior occlusal support forces a mandatory dietary shift away from complex fiber-rich foods (raw vegetables, whole grains, nuts) toward soft, processed carbohydrates [[8](https://doi.org/10.3390/nu14061279)]. Reduced dietary fiber intake depletes gut microbiome production of short-chain fatty acids (acetate, propionate, butyrate), impairing G-protein-coupled receptor (GPR41/GPR43) signaling in vascular smooth muscle and accelerating vascular stiffness and hypertension ($\text{SBP} = 127.61\text{ mmHg}$ in unrestored impairment) [[3](https://doi.org/10.1038/s41440-022-00976-3)].

### 4.3 Periodontal Endotoxemia and Systemic Inflammatory Priming
Periodontitis and untreated molar loss provide a chronic vascular portal for periodontal pathogens (*Porphyromonas gingivalis*, *Treponema denticola*). Translocated lipopolysaccharides (LPS) activate Toll-like receptor 4 (TLR4) on circulating monocytes and vascular endothelial cells, elevating systemic levels of C-reactive protein (CRP), interleukin-6 ($IL-6$), and tumor necrosis factor-alpha ($TNF-\alpha$) [[9](https://doi.org/10.1155/2023/9720947)]. This persistent systemic inflammatory priming accounts for the $68.6\%$ direct effect observed in our causal mediation model.

### 4.4 Biomechanics of Molar Occlusal Support vs. Anterior Guidance
Anatomically, posterior molars absorb high axial masticatory forces ($400 - 800\text{ N}$) and maintain vertical dimension of occlusion (VDO). Anterior teeth serve primarily for incision and anterior guidance under lower force loads ($100 - 200\text{ N}$). Molar loss destabilizes the temporomandibular joint (TMJ), compromises airway patency during sleep, and drastically impairs comminution efficiency, explaining why molar loss carries a 2.34-fold higher hazard of mortality ($\text{HR} = 4.846$) than anterior loss ($\text{HR} = 2.074$).

---

## 5. Clinical & Health Policy Recommendations

1. **Routine Oral Frailty Screening in Cardiology and Endocrinology**: General practitioners and cardiologists should incorporate a simple 1-minute chewing difficulty assessment (`sosyaku_code`) into routine clinical visits for hypertensive and diabetic patients.
2. **Prosthodontic Rehabilitation as Cardiovascular Prevention**: National health insurance frameworks should classify prosthodontic restoration (removable dentures, fixed bridges, dental implants) as an essential preventive medical intervention capable of reducing mortality hazard by $57.2\%$.
3. **Molar Preservation Protocols**: Dental practitioners should prioritize conservative endodontic and periodontal preservation of posterior molars, given that molar loss contributes $28.4\%$ feature importance in predicting 5-year incident CVD events.

---

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