Curcumin has been shown to exert therapeutic or protective effects against a variety of diseases, such as cancer, pulmonary diseases, neurological, liver, metabolic, autoimmune, cardiovascular diseases and numerous other chronic ailments. Over 116 clinical studies on curcumin in humans were registered with the US National Institutes of Health in 2015. However, it is mystifying how curcumin can be so effective in the treatment of many diseases since it has very low water solubility and bioavailability. Furthermore, curcumin is not stable under various conditions; its degradation or condensation into different bioactive compounds may be responsible for its biological activities rather than curcumin itself. In this review, we provide evidence of curcumin degradation and condensation into different compounds which have or may have health benefits themselves. Literature reviews strongly suggest that these molecules contribute to the observed health benefits, rather than curcumin itself.
The mortality rates of cancer patients decreased by ~1.5% per year between 2001 and 2015, although the decrease depends on patient sex, ethnic group and type of malignancy. Cancer remains a significant global health problem, requiring a search for novel treatments. The most common property of malignant tumors is their capacity to invade adjacent tissue and to metastasize, and this cancer aggressiveness is contingent on overexpression of proteolytic enzymes. The components of the plasminogen activation system (PAS) and the metal-loproteinase family [mainly matrix metalloproteinases (MMPs)] are overexpressed in malignant tumors, driving the local invasion, metastasis and angiogenesis. This is the case for numerous types of cancer, such as breast, colon, prostate and oral carcinoma, among others. Present chemotherapeutics agents typically attack all dividing cells; however, for future therapeutic agents to be clinically successful, they need to be highly selective for a specific protein(s) and act on the cancerous tissues without adverse systemic effects. Inhibition of proteolysis in cancerous tissue has the ability to attenuate tumor invasion, angiogenesis and migration. For that purpose, inhibiting both PAS and MMPs may be another approach, since the two groups of enzymes are overexpressed in cancer. In the present review, the roles and new findings on PAS and MMP families in cancer formation, growth and possible treatments are discussed.
Chlorhexidine (CHX) is considered the gold standard in the antiseptic treatment of the oral cavity, due to its high antibactericidal capability. With the use of CHX mouth-rinse formulations, the bacteriostatic effects are maintained by the adsorption and prolonged release of CHX from oral surfaces. It was believed that antiplaque formation ability and the lack of systemic toxicity of CHX render it an excellent antiseptic in post-surgical dental treatment. However, recent studies have demonstrated that CHX exerts cytotoxic effects on human periodontal tissues, such as gingival fibroblasts and other cells. It also reduces gingival fibroblast adhesion to fibronectin and prevents fibroblast attachment to root surfaces, thus interfering with periodontal regeneration. In this study, using human gingival fibroblasts (HGFs), we investigated effects of CHX on the growth, morphology and proliferation of HGFs. We found that a low concentration (0.002%) of CHX does not interfere with the proliferation and morphology of HGFs. However, a higher concentration (≥0.04%) of CHX inhibits cell proliferation and to a certain extent, affects cell morphology in a time-dependent manner. A decrease in the percentage of cells in the G0/G1 phase and the accumulation of cells in the S phase following treatment with CHX also occurred in a dose-dependent manner. We thus concluded that CHX only at the concentration of 0.002% does not interfere with HGF growth, that is so critical to wound healing. Thus, the application of CHX in the post-surgical antiseptic treatment of the oral cavity should be limited.
Introduction: Oral lesions are divided into non-neoplastic lesions, potentially malignant lesions and neoplastic lesions. More clinical data are needed to determine their helpful clinical pattern. Aim: To present the epidemiological, clinical and histopathological characteristics of the oral lesions. Material and methods: The retrospective study group comprised records of 208 patients which were reviewed according to selected epidemiological and clinical features. All the biopsy specimens were classified into: reactive lesions, precancerous lesions/potentially malignant lesions, salivary gland pathologies, benign and malignant tumours. Results: The lower lip was the most common site involved followed by buccal and vestibular mucosa. The most frequent diagnoses were fibroma, mucocele and papilloma. The predominant pathomorphological forms were nodule and bulla. The most frequent salivary gland pathology was mucocele. Fibroma was the most frequent pathomorphological diagnosis, followed by mucocele and reactive lesions such as irritation fibroma (IF) and granuloma. Conclusions: In cases of oral mucosal lesions, we propose the following algorithm: the exclusion of all odontogenic and iatrogenic causes; the detection and elimination of harmful habits, parafunctions and irritants from the oral cavity especially from the vestibule of the oral cavity and from the lips; all surgical treatment should be performed only after the proper detection and elimination of causative factors to decrease the risk of recurrence; excisional biopsy or in more diffuse lesions incisional biopsy is recommended to confirm clinical diagnosis; and consideration of other factors that can modify the clinical pattern of oral lesions, such as oral hygiene, systemic diseases, and drugs.
Recently, many studies have investigated the relationship between the level of metals in the body and various diseases. The objective of this study was to examine any possible influence of periodontal disease upon the concentration of metals in oral fluid and blood and to explore the usability of applying cluster analysis coupled with the analysis of selected elements in oral fluid, calcium (Ca), copper (Cu), iron (Fe), magnesium (Mg), manganese (Mn), zinc (Zn), cadmium (Cd) and lead (Pb), for effectively distinguishing people affected by periodontitis from healthy individuals. The quantification of eight metals in oral fluid and blood samples was performed by two inductively coupled plasma techniques–inductively coupled plasma mass spectrometry (ICP-MS) and inductively coupled plasma optical emission spectrometry (ICP-OES). Most of the examined elements were detected at elevated concentration in the oral fluid of periodontal patients. However, the differences were statistically significant in the case of three metals: Cu, Mg and Mn (p < 0.05). Approximately, fivefold increase in the concentration of Cu, threefold-elevated levels of Mn and a twofold increase in the concentration of Mg were found in the oral fluid of the periodontal patients compared to the controls. Cluster analysis confirmed the statistical significance of the differences in the level of metals in the oral fluid between the two groups in most cases, plus enabled the correct classification of the subjects into patients and controls. The relationship between concentrations of metals and periodontal disease may in the future serve to prevent the development of such disease.
The plasminogen activation system (PAS) plays an essential role in tissue proteolysis in physiological and pathological processes. Periodontitis is a chronic infection associated with increased proteolysis driven by plasminogen activation. In this comprehensive review, we summarise the effects of PAS in wound healing, tissue remodelling, inflammation, bacterial infection, and in the initiation and progression of periodontal disease. Specifically, we discuss the role of plasminogen activators (PAs), including urokinase PA (uPA), tissue-type PA (tPA), PA inhibitor type 1 (PAI-1) and 2 (PAI-2) and activated plasminogen in periodontal tissue, where their concentrations can reach much higher values than those found in other parts of the body. We also discuss whether PA deficiencies can have effects on periodontal tissue. We conclude that in periodontal disease, PAS is unbalanced and equalizing its function can improve the clinical periodontal tissue condition.
The Meckel's cartilage itself and the mandible are derived from the first branchial arch, and their development depends upon the contribution of the cranial neural crest cells. The prenatal development of the Meckel's cartilage, along with its relationship to the developing mandible and the related structures, were studied histologically in human embryos and fetuses. The material was obtained from a collection of the Department of Anatomy, and laboratory procedures were used to prepare sections, which were stained according to standard light-microscopy methods. The formation of the Meckel's cartilage and its related structures was observed and documented. Some critical moments in the development of the Meckel's cartilage are suggested. The sequential development of the Meckel's cartilage started as early as stage 13 (32 days) with the appearance of condensation of mesenchymal cells within the mandibular prominence. During stage 17 (41 days), the primary ossification center of the mandible appeared on the inferior margin of the Meckel's cartilage. The muscular attachments to the Meckel's cartilage in embryos were observed at stage 18 (44 days). Their subsequent movement into the developing mandible during the 10th week seemed to diminish the role of the Meckel's cartilage as the supportive core; simultaneously, the process of regression within the cartilage was induced. During the embryonic period, the bilateral Meckel's cartilages were in closest contact at the posterior surface of their superior margins, preceding formation of the symphyseal cartilage at this site. The event sequence in the development of the Meckel's cartilage is finally discussed.
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