The effects of enamel matrix derivative (EMD; Emdogain) on new trabecular bone induction after pure bioinert titanium (Ti) implantation in the rat femur were examined by means of routine light and transmission electron microscopy, immunohistochemistry, and backscattered electron image analysis. Newly designed mini-Ti implants (3.5 mm in length and 1.6 mm in diameter) were placed in the corticotrabecular area of the femur with either EMD or its carrier, propylene glycol alginate, as control. On post-implantation days 4, 7, 14, and 30, the dissected femur was examined in the transverse direction through Ti implants. In both control and EMD-applied femurs, trabecular bone formation was recognized over the implant surfaces and within medullary cavities even at 4 days post-implantation. These newly formed bone trabeculae around the Ti implants were immunoreactive for bone sialoproteins as a bone matrix marker, and osteoclastic bone resorption became evident in these bone trabeculae after 7 days post-implantation. Although trabecular bone area around the implants was markedly decreased at 30 days post-implantation compared with those at 14 days, the trabecular bone areas in EMD-applied femurs were significantly greater than those in propylene glycol alginate-applied femurs at both 14 and 30 days post-implantation. Our results suggest that EMD is an effective biological matrix for enhancing new trabecular bone induction and resulting attachment of orthopedic prostheses to the recipient bone.

We examined the biological effects of porcine enamel matrix derivative (EMD; Emdogain) on the formation of reparative dentine and dentine bridges in rat molars after pulp amputation. The pulp chambers of upper molars of Wistar rats were perforated and the amputated pulp surfaces were directly capped with either EMD or its carrier propylene glycol alginate (PGA) as control. The cavities were then restored with glass-ionomer cement. On post-amputation days 4-30, the dissected maxillae were examined by light and electron microscopy. In PGA-capped pulp, reparative dentine had been formed over the dentine walls under the prepared cavity on day 7 post-amputation and its thickness extended until day 30. On day 30, as well as reparative dentine formation, diffuse calcification had occurred beneath the amputated wound surfaces. Dentine bridge formation under the amputated coronal pulp surface was observed in 18.2% of amputated pulp on day 30. In EMD-capped pulp, reparative dentine had already been formed by odontoblast-like cells over the dentine walls, already on day 4 post-amputation, and its thickness extended until day 30. The Ca and P weight % and Ca/P ratio of reparative dentine matrix were similar to those of pre-existing dentine matrix, and these values were not different between PGA and EMD-capped pulp. Dentine bridge formation was observed in 27.3% of EMD-capped pulp on day 30. Our results suggest that EMD enhances the formation of both reparative dentine and dentine bridges during wound healing of amputated rat molar pulp.

Osteoprotegerin (OPG) is a novel osteoblast-derived secreted member of the tumour necrosis factor receptor superfamily that inhibits osteoclastogenesis. We examined the effects of OPG administration on the distribution, ultrastructure and vacuolar-type H+-ATPase expression of osteoclasts and resulting trabecular bone loss in the femurs of ovariectomized (OVX) mice. Two-month-old female ddY mice were allocated to the following groups: (1) pretreatment base-line controls; (2) untreated sham-operated controls; (3) untreated OVX; and (4) OPG-administered OVX mice. Postoperatively, OPG (0.3 mg kg(-1) day(-1)) was intraperitoneally administered daily to OVX mice for 7 days. On postoperative day 7, all mice were sacrificed, and the dissected femurs were examined by means of light and immunoelectron microscopy and quantitative backscattered-electron image analysis. Backscattered-electron examination revealed that trabecular bone area/unit medullary area in untreated OVX mice was significantly lower than that of base-line control and sham-operated control mice. Compared with untreated OVX mice, OPG administration to OVX mice significantly increased trabecular bone area, which was similar to that of sham-operated control mice. Surprisingly, the number of TRAP-positive osteoclasts along the trabecular bone surfaces in OPG-administered OVX mice was not significantly decreased compared with that of sham-operated control and untreated OVX mice. Ultrastructurally, OPG administration caused disappearance of ruffled borders in most osteoclasts, but induced neither necrotic nor apoptotic changes. In addition, the expression of vacuolar-type H+-ATPase in osteoclasts was decreased by OPG administration. Our results suggest that low-dose OPG administration significantly reduces trabecular bone loss in OVX mice via impairment of the structure and bone resorbing activity of osteoclasts.

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