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Scientific evidence that has been gathered in the past 20 years established that certain endosseous dental implants--primarily screw-type implants made of commercially pure titanium can be successfully utilized as anchorage for dental prostheses. In recent years, an effort has been made to simplify the surgical procedure, in order to modify clinical treatment modalities. One of the trends is to increasingly utilize microrough titanium implants. Roughened implant surfaces have a long history in implant dentistry, and the most prominent surface is titanium plasma-sprayed (TPS). In recent years new implant surfaces have emerged, so-called microrough titanium surfaces produced with reducing techniques such as grit-blasting with Al2O3 or TiO2 particles, sandblasting and acid-etching, or acid-etching alone. These different titanium surfaces have been tested in numerous in-vivo studies utilizing different animal models. Summarizing the results of these studies, it can be concluded that there is currently sufficient evidence that titanium implants with a microrough surfaces achieve a faster bone integration, a higher percentage of Bone implant Contact (BIC), and a higher resistance to shear documented with higher Removal Torque Values (RTV) when compared with titanium implants with a polished or machined surface. In order to understand the mechanism through which surface roughness modulates its effects mentioned above, recent studies used in-vitro experimental methods to study cell response to implant surface topography. These studies have shown that osteoblasts are sensitive to surface roughness, exhibiting decreased proliferation and a more differentiated phenotype on rougher surfaces. PGE2 production is enhanced on rough surfaces, as is the production of TGF beta 1, suggesting that surface roughness can mediate autocrine and paracrine regulation of osteogenesis. Moreover, surface roughness was found to modulate the effect of systemic hormones like 1,25-(OH)2D3 on osteoblasts. The clinical advantages of implants with rough surface were observed in recently conducted clinical trials. It was found, in humans, that roughened titanium implants need shorter healing period before loading, 6-8 (SLA and Osseotite respectively) weeks instead of 12 weeks. The clinical advantages of shorter healing periods are obvious. Moreover, it was found that certain roughened implants can be used in shorter sizes (6-8 mm) then accepted today. The utilization of shorter implants offers the avoidance of extensive surgical procedures such as nerve lateralization in the mandible or sinus grafting in the maxilla. However, sufficient long term documentation is still lacking, and the predictability of such modalities has yet to be examined in long term prospective clinical trials.

Matrix Metaloproteinases (MMPs) play a crucial role in the pathogenesis of the periodontal disease. This group of enzymes can degrade most of the proteins that compose the extracellular matrix. Recently a new concept of treatment, the "host modulating therapy" (HMT) was developed. The rationale behind this concept is to inhibit the production of the inflammatory mediators and/or to block the production of the host MMPs and thus inhibiting disease production. In the recent years it was found that Tetracyclines (TC) decrease the levels of TNF-alpha, IL-1, Nitric Oxide, and prostaglandins, and via intra and extra cellular mechanisms inhibit the production and activation of the MMPs. A capsule of 20 mg Doxycycline, called later Low Dose Doxycycline (LDD), was the first HMT in the periodontal disease. In a 9 month study it was found that LDD bid after supragingival scaling statistically increased pocket reduction and attachment gain compared to supragingival scaling alone. However, this improvement was found only in pockets of 7 mm or more, and was not compared yet to periodontal supportive therapy every three month. There is a need for more basic and clinical research in the field of HMT in the treatment of periodontal disease, to expand our knowledge and clinical experience that will enable us to decide when and how to use medications to modulate host response.

Purpose: To assess whether coverage of an untreated or restored carious root lesion with a subepithelial connective tissue graft would provide a predictable, esthetically acceptable result and prevent further caries progression., Materials and Methods: Twenty-seven teeth from 13 patients with root caries and gingival recessions of 3.4 +/- 0.2 mm (mean +/- SEM) were treated with subepithelial connective tissue grafts. Eighteen teeth had untreated caries, and the other nine had composite or glass-ionomer restorations. The carious dentin and the plastic restorations were removed prior to the surgical procedure. The exposed roots were thoroughly planed and covered by a subepithelial connective graft with no further root treatment or conditioning. The teeth were examined periodically from 1-6 years post-treatment for retention of root surface coverage and presence of carious lesions., Results: The mean root coverage recession left after the treatment was 0.3 +/- 0.1 mm, with coverage of 92.4 +/- 2.4%. Significant differences (P< 0.05) were found between the coverage of roots with carious lesions that had not been restored and those that had restorations removed. However, since the number of teeth with restorations was limited, further study is required to confirm this difference. In 18 cases, complete coverage of the recession was achieved. The results were stable, and no further recessions or recurrent caries were detected.

Parathyroid hormone (1-34) (PTH(1-34) and transforming growth factor-beta1 (TGF-beta1) regulate chondrocyte proliferation, differentiation, and matrix synthesis. Both proteins mediate their effects in a dose- and time-dependent manner, and the effects are cell maturation specific. Moreover, similar signaling pathways are used, suggesting that there may be cross talk leading to coregulated cell response. To test this hypothesis, confluent cultures of rat costochondral resting zone and growth zone chondrocytes were treated with 0.22, 0.44, or 0.88 ng/mL of rhTGF-beta1 for 24 h, followed by treatment with 10(-11) to 10(-8) M PTH(1-34) for 10 min or 24 h. [3H]-Thymidine incorporation, specific activity of alkaline phosphatase (AP), and [35S]-sulfate incorporation were measured. PTH(1-34) had no effect on [3H]-thymidine incorporation by growth zone cells pretreated with 0.22 or 0.44 ng/mL of TGF-beta1, but in cultures treated with 0.88 ng/mL, PTH(1-34) caused a dose-dependent decrease that was maximal at the lowest concentration tested. By contrast, PTH(1-34) stimulated [3H]-thymidine incorporation by resting zone cells, and this effect was additive with the stimulation caused by 0.22 ng/mL of TGF-beta1. PTH(1-34) caused a synergistic increase in AP in growth zone cells treated with 0.44 or 0.88 ng/mL of TGF-beta1, but not in cells treated with 0.22 ng/mL of TGF-beta1. It had no effect on AP in resting zone cells pretreated with any concentration of TGF-beta1. PTH(1-34) increased [35S]-sulfate incorporation in growth zone and resting zone cell cultures treated with 0.22 ng/mL of TGF-beta1 to levels seen in cultures treated with 0.88 ng/mL of TGF-beta1 alone. These results support the hypothesis that PTH(1-34) and TGF-beta1 coregulate growth plate chondrocytes and that the effects are cell maturation dependent.

This study examined the interrelationship between transforming growth factor-beta1 (TGF-beta1) and 17beta-estradiol (E2) in the regulation of growth plate chondrocytes. To determine whether TGF-beta1 modulates chondrocyte response to E2, we used cells isolated from the resting zone (RC) and growth zone (GC) of costochondral cartilage. Confluent, fourth-passage cultures were pretreated with rhTGF-beta1 for 24 h, followed by treatment with E2 for 24 h. The effect of TGF-beta1 and E2 alone, or the sequential combination, were examined by measuring [3H]-thymidine incorporation (proliferation), alkaline phosphatase (AP) specific activity (differentiation), and [35S]-sulfate incorporation (matrix synthesis). TGF-beta1 alone increased [3H]-thymidine incorporation in both female and male RC and GC cells, but E2 affected this parameter only in RC cells, causing a dose-dependent decrease. At the highest concentration of TGF-beta1 and E2, [3H]-thymidine incorporation in female GC cells was the same as seen in untreated control cultures. In male GC cells, [3H]-thymidine incorporation in cultures treated with TGF-beta1 and E2 exhibited a comparable increase, as was seen in cultures treated with TGF-beta1 alone. TGF-beta1 caused a biphasic stimulation in AP that was maximal at 0.22 ng/mL, in both female and male RC and GC cells. E2, however, affected only female cells. Whereas the effect of TGF-beta1 predominated in RC and GC male cells, the biphasic stimulation caused by E2, maximal at 109 M, predominated in female RC cells. In female GC cells, however, TGF-beta1 caused a synergistic response, resulting in enhanced AP specific activity in cultures pretreated with 0.22 ng/mL of TGF-beta1 and 10(-8) M E2. TGF-beta1 alone caused dose-dependent increases in [35S]-sulfate incorporation in female RC and GC cells, as well as in male GC cells, but had no effect on male RC cells. E2 affected only female cells. TGF-beta1 potentiated the effect of E2 on this parameter, resulting in synergistic increases in the female cells. This is the first demonstration of a gender-specific response to TGF-beta1 in chondrocytes. These results suggest that chondrocyte response to a systemic hormone such as E2 can be modulated by local regulatory agents such as TGF-beta1.

Bell's palsy is a sudden, isolated, peripheral facial paralysis caused by various known and sometimes unknown factors. The case of an 18-year-old man who developed Bell's palsy after onset of primary herpetic gingivostomatitis is presented. Although Bell's palsy has already been associated with herpes simplex virus type 1, the described case is the first in the literature in which enzyme-linked immunosorbent assays for immunoglobulin G to herpes simplex virus type 1 and herpes simplex virus type 1 culture were both positive. The recent literature regarding the possible relationship between herpes simplex virus type 1 and Bell's palsy is reviewed and discussed.

Recently, sex hormones were shown to stimulate chondrocyte differentiation and matrix protein synthesis in vitro in a sex-specific and maturation-dependent manner. The aim of the present study was to determine whether cytosolic receptors in these cells would specifically bind 17 beta-estradiol and testosterone, and if so, whether binding was gender- and maturation-dependent. Confluent, fourth passage cultures of cells derived from male or female rat costochondral growth zone and resting zone cartilage were homogenized and specific binding of 17 beta-estradiol or testosterone measured in the cytosolic fraction. Scatchard analysis indicated the presence of a high-affinity 17 beta-estradiol receptor (Kd = 4.5 to 8.7 x 10(-11) M), with low binding capacity (3.9 to 11.2 fmol/mg protein). Chondrocytes from female rats were found to have a significantly greater binding capacity for 17 beta-estradiol than chondrocytes from male rats. However, cells from both sexes had binding capacities that were independent of cell maturation. A high-affinity testosterone receptor (Kd = 4.3 to 6.3 x 10(-11) M) with low binding capacity (4.1 to 5.9 fmol/mg protein) was found in both males and females, but no difference in binding capacity was noted, either as a function of gender or stage of cell maturation. Immunohistochemistry using antibodies against 17 beta-estradiol and testosterone and the 17 beta-estradiol nuclear receptor (D-75) confirmed that 17 beta-estradiol and testosterone receptors were present in chondrocytes from both male and female rats. These data demonstrate that chondrocytes from growth zone and resting zone cartilage are capable of binding both 17 beta-estradiol and testosterone. This suggests that these hormones mediate their direct effects on chondrocytes via receptors specific for their appropriate ligand. The sex-specific effects of 17 beta-estradiol may be due to differences in receptor number between chondrocytes derived from female and male rats. In contrast, the sex-specific effects of testosterone may be regulated at the post receptor level since no differences in binding capacity were found between males and females.