Association between Sjögren syndrome and osteoporosis: A bidirectional Mendelian randomization study

Qian Zhao; Jiahong Li; Jing Zou; Guocui Wei; Yanping Wang; Xiuxia Li; Xuan Xiong

doi:10.1097/md.0000000000043072

July 18, 2025MedicineOpen Access

Association between Sjögren syndrome and osteoporosis: A bidirectional Mendelian randomization study

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Why the study?

The study aimed to investigate the bidirectional causal relationships between Sjögren syndrome and osteoporosis using genetic instruments.

Is there a bidirectional causal relationship between Sjögren syndrome and osteoporosis?

Structured PICO

Is there a bidirectional causal relationship between Sjögren syndrome and osteoporosis?

P

Population

Genetic instruments for predisposition to Sjögren syndrome (SS) and osteoporosis (OP) from published genome-wide association studies

I

Intervention

Genetic predisposition to Sjögren syndrome (SS)

C

Comparator

Genetic predisposition to osteoporosis (OP) for reverse causality analysis

O

Outcome

Association between Sjögren syndrome and osteoporosis

Genetic predisposition to Sjögren syndrome is a risk factor for osteoporosis, but there is no reverse causality.

Implication

SS may genetically increase OP risk; leaves open whether screening or interventions warrant clinical testing.

Abstract

This Mendelian randomization (MR) study aimed to investigate the relationships between Sjögren syndrome (SS) and osteoporosis (OP). We selected genetic instruments for predisposition to SS on published genome-wide association studies. Using a two-sample MR approach, we assessed association SS and OP. The random effects inverse variance weighting method was used as the primary analysis method, and the weighted median method, MR-Egger, weighted mode, and simple mode were used as supplementary analytical methods. Sensitivity analysis was performed using the heterogeneity test, the pleiotropy test, and the leave-one-out test. SS was notably associated with the presence of OP (odds ratio: 1.191; 95% confidence interval: 1.084-1.309; P < .005), but OP was not a susceptible factor for SS. This study suggested that from a genetic point of view, the SS was indeed a risk factor for OP. Furthermore, no significant causal effect of OP on SS was observed, indicating the absence of reverse causality between SS and OP.