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. 2019 Apr 10;98(6):689–697. doi: 10.1177/0022034519839438

Figure 2.

Figure 2.

Hyperloading causes local apoptosis in the periodontal ligament (PDL), followed by robust proliferation. (A) Pentachrome staining of a representative sagittal tissue section through mnM1 from mice with intact dentition. (B) Higher magnification of boxed area in panel A. (C) Periostin immunostaining of the PDL. (D) Representative sagittal section through mnM1 after 7 d of hyperloading caused by extraction of the opposing dentition. (E) Higher magnification of boxed area in panel D. (F) Periostin immunostaining of the PDL. (G) Quantification of cell density in the PDL of the furcation area. (H) Quantification of PDL width from immunostaining staining and µCT data. (I–L) Cell apoptosis detected by TUNEL staining and (M–P) cell proliferation detected by PCNA immunostaining in the PDL at time points indicated. (Q) Quantification of TUNEL+ve (n = 3) and PCNA+ve cells (n = 3) in the furcation PDL, as a function of time. Immunostaining for type I collagen in the PDL of mice with (R) intact dentition and (S) following 28 d of hyperloading. Scale bars = 50 µm. Values are presented as mean ± SD. *P < 0.05. **P < 0.01. ab, alveolar bone; d, dentin; PCNA, proliferating cell nuclear antigen; µCT, micro–computed tomography.