The hair follicles (HFs) and the interfollicular epidermis (IFE) of intact mature skin are maintained by distinct stem cell populations. Upon wounding, however, emigration of HF keratinocytes to the IFE plays a role in acute stages of healing. In addition to this repair function, rapidly cycling cells of the upper HF have been observed transiting to the IFE in neonatal skin. Here we report that an absence of HF development leads to shortening and kinking of the mouse tail. These skeletal defects are reduced by stimulating keratinocyte proliferation, suggesting that they arise from impaired epidermal expansion. We confirm that rapidly cycling cells of the HF emigrate to the IFE of the neonatal tail. These results suggest that an absence of HFs results in impaired skin growth that is unable to keep pace with the rapidly elongating axial skeleton of the tail. Thus, in addition to their role in wound repair, HFs can make a significant contribution to lateral expansion of the IFE in the absence of trauma.