Razvan Liviu Petre

Temporomandibular disorders (TMD) are the most common cause of non-dental orofacial pain, affecting about 1/3 of the population worldwide. The Diagnostic Criteria for Temporomandibular Disorders (DC/TMD) Axis I is recognized as the international gold standard for the clinical and research diagnosis of TMD; however, no validated Romanian version has been available to date. The aim of the present study was to translate and culturally adapt the DC/TMD Axis I into Romanian, and to evaluate its criterion validity and interand intra-examiner reliability. This cross-sectional methodological study followed the Beaton et al. and DC/TMD translation guidelines. The process included forward-backward translation, an expert panel review, and pre-testing on 20 patients to ensure semantic and conceptual equivalence. A total of 140 Romanian-speaking adults (mean age: 34.7 ±12.1 years; 70.7% women) were examined by 2 calibrated clinicians. Criterion validity was assessed against an expert-consensus reference diagnosis. Interand intra-examiner reliability for categorical variables was analyzed using Cohen's κ, and for continuous measurements using intraclass correlation coefficients (ICCs). The Bland-Altman plots and demographic analyses further evaluated measurement consistency. The Romanian DC/TMD Axis I showed excellent diagnostic performance, with sensitivity ranging from 85.7% (for disc displacement without reduction) to 91.2% (for myalgia), specificity of 93.5-98.2%, and AUC (the area under the receiver operating characteristic (ROC) curve) ≥ 0.91 for all diagnostic categories. Inter-examiner agreement was substantial to almost perfect (κ = 0.78-0.94), and intra-examiner agreement similarly high (κ = 0.80-0.95). Continuous mandibular measurements demonstrated excellent reproducibility (ICC = 0.89-0.96). Slightly lower sensitivity for disc displacement without reduction indicates an area for further refinement of diagnostic criteria. The Romanian version of the DC/TMD Axis I is a valid, reliable and culturally equivalent tool for diagnosing TMD. Its adoption will standardize clinical assessment, enhance interdisciplinary communication, and enable Romanian participation in multicenter and educational initiatives across Central and Eastern Europe.

Exercise adaptation depends on a dynamic alternation between catabolic and anabolic states coordinated primarily by AMP-activated protein kinase (AMPK) and mechanistic target of rapamycin (mTOR). While transient activation of these pathways underpins beneficial molecular remodeling, the system-level consequences of sustained anabolic drive remain insufficiently conceptualized in exercise biology. This article presents a conceptual mechanistic narrative review integrating evidence from molecular nutrition, exercise physiology, redox biology, and epigenetic regulation to define limits of adaptive signaling. We propose the Metabolic Overdrive Model, a systems-level framework describing the transition from adaptive AMPK–mTOR oscillation to a high-anabolic lock-in state characterized by persistent mTORC1 activation, suppressed AMPK signaling, altered NAD⁺ economy (SIRT1–PARP imbalance), redox dysregulation, and progressive epigenetic drift. Using exercise and training as models of sustained metabolic stress, we synthesize mechanistic parallels across energy sensing, oxidative signaling, and chromatin regulation without implying pathological causality. The framework generates testable predictions linking prolonged post-exercise anabolic signaling (>24 h) to specific molecular signatures, including AMPK phosphorylation status, NAD⁺ availability, PARylation, histone acetylation, and DNA methylation dynamics. By reframing exercise adaptation as a loss-of-oscillation phenomenon rather than a linear continuum, this model provides a mechanistic language for hypothesis generation, biomarker-guided periodization, and future experimental validation.

Elite performance relies on a rhythmic alternation between catabolic and anabolic states orchestrated by AMPK and mTOR. We propose that chronic nutrient or hormonal stimulation can flatten this oscillation and induce a metabolic overdrive state characterized by sustained mTORC1 activation, suppressed autophagy, redox imbalance, and NAD⁺‑dependent silencing of SIRT1 via PARP overactivation, with downstream epigenetic drift. We present a conceptual mechanistic narrative review integrating evidence from molecular nutrition, exercise physiology, and cancer biology into a systems framework linking AMPK–mTOR dynamics, the SIRT1–PARP NAD⁺ economy, and chromatin regulation (DNMT/TET, HAT/HDAC, miRNAs). Using elite sport as a natural model of maximal adaptation, we outline mechanistic parallels—not causal equivalence— between performance enhancement and pro‑proliferative signaling. We define testable predictions: (1) prolonged mTORC1 activation (>24 h post‑exercise) associates with ↓AMPK Thr172‑P, ↓NAD⁺ and ↓SIRT1 activity; (2) overreaching with high anabolic load increases PARylation and H3K9ac while reducing TET activity; (3) interventions that periodically restore AMPK (fasted endurance, time‑restricted feeding, polyphenol‑mediated AMPK activation) re‑establish oscillation and reduce redox/epigenetic noise. The Metabolic Overdrive Model provides a mechanistic language for the molecular limits of exercise adaptation and a basis for biomarker‑guided periodization that preserves resilience. No causal inference is claimed.