High-energy laser irradiation has been shown to cause crystalline transformations in apatites, which may lead to the formation of tricalcium phosphates with a resulting decrease in acid resistance. Depending on the nature and energy density of laser irradiation used, however, an increase of acid resistance of dental enamel has also been reported after laser irradiation. The aim of the present study was to investigate the phase transformation of hydroxyapatite (HA) to fluorapatite (FA) in a model system that incorporates sodium fluoride (NaF) into apatite structure by using laser irradiation. A CO2 laser was used at energy densities ranging from 21 to 500J/cm2. Synthetic HA mixed with NaF (10:1) was the target of laser irradiation. The crystalline structures were then investigated using X-ray diffraction analysis. The results showed that a phase transformation of HA to FA could be realized, and that the threshold energy density needed was 38 J/cm2. Not only is the finding crystallographically important, but it also opens new perspectives for future research regarding the development of laser technology for clinical purposes.
The distribution of the extracellular matrix glycoprotein, tenascin, was studied in normal mucosa and during healing of scalpel incised or excised and CO2 laser-wounded rat tongue dorsal mucosa in 51 male Sprague-Dawley rats over a period of 21 days. A polyclonal antibody specific for tenascin was applied in indirect immunofluorescence microscopy. In normal mucosa tenascin was sparsely distributed in a discontinuous manner at the tips of the connective tissue papillae in association with the basement membrane (BM) and in the walls of the capillaries. In all the healing wounds there was a marked increase in the distribution of tenascin, particularly close to the BMs at the wound edges beneath the proliferating and migrating epithelium, and later on during healing in the regenerating connective tissue (CT) area. This expression subsided later on during healing. Laser surgery did not alter the ability of fibroblasts to synthesize tenascin. The transient expression of tenascin in the BMs and CT of the healing wounds suggests that this protein could play an important role in providing ideal conditions for cell movement, and in the deposition and organization of other extracellular matrix (ECM) glycoproteins during tissue repair.
Extracellular matrix components laminin, Type IV collagen, Type III collagen, and fibronectin, of laser‐treated rat tongue mucosa were studied over a healing period of 28 days by using immunohistochemical and electron microscopic techniques. Their distribution and amount in laser wounds was compared with that in scalpel incisions and normal tongue mucosa. Laser treatment caused an extensive destruction of both epithelial and stromal cells but left much of the connective tissue matrix intact. Basement membranes, in particular, appeared to resist laser irradiation. During the study period the laser‐induced lesions healed through reparative synthesis of matrix proteins which led to filling of the tissue defects. The regenerative processes with concomitant re‐epithelialization took place more slowly in laser‐treated than in scalpel incision wounds. The relative resistance of the matrix proteins against laser irradiation and the slow removal and replacement of the residual matrix is suggested to account at least partially for the lack of scarring and contraction frequently observed in laser‐treated areas.
The distribution of the extracellular matrix (ECM) protein tenascin (Tn) was studied in oral premalignant lesions and squamous cell carcinoma by using the monoclonal antibody (Mab) 143DB7. In normal buccal and palatal mucosa, in ventral tongue, in floor of mouth and in gingiva, immunoreaction for Tn was seen to be distributed as a continuous thin, delicate line merely in the basement membrane region. Hyperkeratosis without dysplasia showed a distinct zone of enhanced Tn immunoreactivity immediately beneath the epithelium. In dysplasias of various degree, enhancement of the stromal Tn content could be observed, being most conspicuous in carcinoma in situ lesions. In most invasive carcinoma cases the Tn immunoreactivity was intense, extending deeply into the underlying stroma. In such lesions Tn-reaction often covered the total stroma. Notably, the strongest immunoreaction was seen at the advancing edges of the tumor. The triggering factor for stromal Tn enhancement seems to be of epithelial origin. The enhanced expression of Tn suggests that Tn plays a role in organizing and remodelling the stroma to support active epithelial proliferation and migration. However, it also seems that inflammation is associated with Tn expressions.
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