Background: Temporomandibular disorders (TMD) exhibit a marked female predominance, suggesting a potential role for estrogen in their pathophysiology. However, the evidence linking estrogen status to TMD risk and symptom severity remains inconsistent across studies. Objective: To systematically review and synthesize the available evidence on the association between estrogen status—including hormonal contraceptive use, menopausal status, menstrual cycle variation, pregnancy, and estrogen receptor gene polymorphisms—and the prevalence and clinical features of TMD in women. Methods: A comprehensive search of PubMed, Embase, Scopus, Web of Science, and Google Scholar was conducted through September 2025. Observational studies involving women diagnosed with TMD using validated diagnostic criteria (RDC/TMD, DC/TMD, or equivalent) and reporting estrogen-related exposures were included. Two independent reviewers conducted study selection, data extraction, and risk-of-bias assessment using the Newcastle-Ottawa Scale (NOS). Due to heterogeneity in exposure definitions and outcome measures, a narrative synthesis was performed. Meta-analysis was not conducted due to insufficient homogeneity across studies. Results: Seven studies met the inclusion criteria, comprising six clinical studies involving 2,735 participants and one mechanistic supportive study involving 18 participants. Two high-quality clinical studies—a prospective cohort and a cross-sectional study—reported quantitative effect estimates: hormonal contraceptive use was associated with an increased risk of first-onset TMD (OR 1.37, 95% CI 1.13–1.66) and concurrent TMD symptoms (OR 1.20, 95% CI 1.06–1.35), while climacteric status was associated with increased odds of TMJ palpation pain (OR 2.64, 95% CI 1.12–6.21), crepitus (OR 2.92, 95% CI 1.13–7.56), and degenerative joint disease (OR 2.27, 95% CI 1.05–4.91). Additional moderate-quality studies provided qualitative evidence supporting associations between menopausal status and TMD prevalence, menstrual cycle–related symptom variation, pregnancy-related symptom modulation, and estrogen receptor gene polymorphisms with TMD susceptibility. According to GRADE criteria, the certainty of evidence was rated as moderate for hormonal contraceptive use and menopausal/climacteric status, and low to very low for the remaining exposure categories due to inconsistency, indirectness, and imprecision. Conclusions: Current evidence suggests that hormonal factors, particularly hormonal contraceptive use and menopausal status, are associated with TMD risk and symptom presentation. However, the limited number of high-quality studies, heterogeneity in exposure definitions, and variability in diagnostic criteria constrain definitive conclusions. Further well-designed prospective cohort studies with standardized diagnostic protocols and biochemically validated hormonal assessments are needed to clarify causal relationships and inform clinical decision-making.