A disintegrin and metalloproteinase with thrombospondin motifs 7 (ADAMTS‑7) has been revealed to serve an important role in inflammation‑associated diseases. However, the role of ADAMTS‑7 in spontaneous abortion (SA) remains unclear. In the present study, human and mouse decidual tissues were used to detect the expression of ADAMTS‑7 and cartilage oligomeric matrix protein (COMP) in mice with lipopolysaccharide (LPS)‑induced abortion (10 mice/group), and in SA humans and the corresponding control group (21 participants in the SA group and 15 participants in the control group). The results revealed that ADAMTS‑7 expression was upregulated and that COMP expression was downregulated in the mouse decidual tissue of the LPS‑induced abortion group, when compared with that of the normal control group. The results were further confirmed by western blot analysis and reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) analysis, which revealed increased ADAMTS‑7 and decreased COMP expression at the protein and mRNA levels in mice treated with LPS. Additionally, the expression of ADAMTS‑7 was negatively correlated with the expression of COMP in mice, with a correlation coefficient of ‑0.936 (P<0.001). In addition, the expression of ADAMTS‑7 and COMP exhibited was similar in the decidual tissue of SA patients when compared with the levels observed in the tissues of the normal control participants, as demonstrated by increased ADAMTS‑7 expression and decreased COMP expression. Western blotting and RT‑qPCR analysis revealed that ADAMTS‑7 was increased and COMP was decreased in the decidual tissue of SA subjects. The correlation analysis of ADAMTS‑7 and COMP in human decidual tissue also revealed a similar result, with a correlation coefficient of ‑0.836 (P<0.001). The results of the present study demonstrated that ADAMTS‑7 was upregulated and COMP was downregulated in the decidual tissues of humans and mice with SA, and a negative correlation was identified between the expression levels of ADAMTS‑7 and COMP, thereby providing novel evidence for a better understanding of the pathogenesis of SA, which may lead to improvements in the clinical pregnancy outcomes of these individuals.