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. Author manuscript; available in PMC: 2015 Apr 6.
Published in final edited form as: Evol Dev. 2005 Sep-Oct;7(5):440–457. doi: 10.1111/j.1525-142X.2005.05048.x

Fig. 6.

Fig. 6

Differentiation defect in K14-Noggin incisors. (A, B) Epithelium–mesenchyme interface of the P1 WT (A) and K14-Noggin (B) M1 incisors from the labial side. Unlike WT incisors, K14-Noggin incisors remain less differentiated. They do not form a distinct layer of polarized ameloblasts and there is no dentin or enamel deposition. Epithelium–mesenchyme interface is uneven and wavy. (C–J) Absence of the tooth-specific differentiation markers in the early postnatal (P1) K14-Noggin incisors. Amelx is strongly expressed in the ameloblasts of the WT incisors (C, D). In WT P1 molars Dspp has distinct expression (G). Dspp is expressed in the preodontoblasts and odontoblasts, as well as in the preameloblasts of the proximal labial side (H). In K14-Noggin P1 incisors, both Amelx (E, F) and Dspp (I, J) are largely absent. (K, L) Epithelium–mesenchyme interface of the P14 WT (K) and K14-Noggin (L) M1 incisors from the labial side. K14-Noggin incisors remain poorly differentiated. Epithelium–mesenchyme interface is uneven and wavy. Section plane: sagittal (A–L). Scale bars: 100 μm (A–L). am, ameloblasts; dp, dermal papilla; od, odontoblasts; pam, preameloblasts; pod, preodontoblasts; pd, predentine; si, stratum intermedium.