Plant cell adhesion is essential for development and stress response, mediated by pectin-rich middle lamella deposition between cell walls. However, the precise control mechanism of cell adhesion remains unclear. The qua2-1 and esmd1-1 mutants provide a better understanding of this process and suggest a signaling pathway triggering the loss and restoration of adhesion via cell wall modifications. This study attempts to characterize the potential regulatory role of endogenous oligogalacturonides (OGs) and pectin modifications in the control of cell adhesion in Arabidopsis. From dark-grown hypocotyls, our extraction revealed seven distinct endogenous OGs with varying polymerization and modifications. Abundance variations of OGs were observed among wild type, qua2-1, esmd1-1, and qua2-1/esmd1-1 mutants. The structure of homogalacturonans was analyzed by enzymatic fingerprint, in order to identify changes in esterification patterns. Expression analysis of pectin-modifying enzymes showed significant variations in PME, PMEI, and PAE genes. Gene expressions correlate with homogalacturonans modifications and cell adhesion phenotypes. This study enhances our understanding of a feedback loop between the endogenous OGs, homogalacturonans esterification fine tuning, and pectin remodeling enzymes expression in controlling cell adhesion.