Apple Replant Disease (ARD) occurs after planting on a site that previously supported the same or closely related species of the subfamily Maloideae (apples, pears). It is caused by soil-borne fungal and/or bacterial microorganisms. Typical symptoms are: (i) speckled, brownish appearance of the root system, (ii) stunting of the shoot, (iii) temporal dormancy of the apical bud and (iv) decrease in leaf surface. The objective of our study was to assay whether the exudation of the dihydrochalcone phloridzin (phloretin-2'-O-β-D-glucosid) via roots of apple seedlings (Malus × domestica Borkh.) is related to onset and development of ARD. Phloridzin is a phenolic compound specific to Malus spp. As a constituent of root exudates with a potential influence on microbial activity, it may affect the microbial population in soil, including pathogenic rhizosphere organisms, in at least two ways: first, as defense factor directed against infection, and second, as a substrate for specialized soil microorganisms. In a pot trial, root exudates of apple seedlings were collected every 9th day over a period of 4 to 16 weeks after transplanting of healthy apple seedlings either into an orchard soil conductive to ARD, or, into the same soil previously sterilized by γ-radiation. Phenolic compounds of the root exudates were collected and analysed using an HPLC system equipped with a reversed phase column and a diode array detector. The results suggest that phloridzin generally occurs in apple root exudates of both healthy and infected plants. The exuded amount increased with total root exudation. Considering particular plant ages, a remarkable difference in root exudation between healthy and infected seedlings could be observed 4 weeks after transplanting. At this early stage of plant development ARD infected seedlings exuded significantly higher amounts of phloridzin compared to healthy seedlings. This could be part of a general defense mechanism of apple seedlings in which phloridzin acts as a phenolic compound with probable toxic properties to microorganisms. The response was clearly ineffective in defense against pathogens causing ARD since infected plants finally showed all typical symptoms of ARD. The fact that phloridzin occurs generally in root exudates may contribute to this ineffectiveness: Specialized pathogens may have adapted to phloridzin or may even use it as a substrate. Unfortunately, little is known about possible plant-pathogenic microorganisms within this context. In conclusion, our results suggest that phloridzin exudation may affect onset and development of ARD infection as an attractant substance to specialized (pathogenic) microorganisms. Moreover, its exudation into the rhizosphere might be influenced by ARD pathogens during the infection process since phloridzin exudation was increased in infected plants compared to healthy apple seedlings of the same developmental stage. To confirm these results, apple rootstock varieties differing in phloridzin exudation should be tested for their susceptibility to ARD.