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    ABSTRACT: There is an increasing global trend in cardiometabolic disorders being a leading cause of morbidity and mortality. Adverse dietary habits and sedentary lifestyles contribute to cardiovascular disease (CVD) and diabetes mellitus (DM). Dietary nutrients in nuts have attracted attention in recent literature due to their beneficial effects on CVD by attenuating lipid profiles, inflammation and oxidative stress. There is well-established evidence of the pharmacological properties of micronutrients that render them therapeutically effective in chronic inflammatory diseases. Although caution should be exercised in using antioxidant supplementation, antioxidant foods as dietary components play an important role in the management of cardiometabolic disorders. There is documented evidence of disease-modifying effects of nutritional compounds with anti-inflammatory and antioxidant effects. They have specific applications in ameliorating oxidative stress- induced inflammatory diseases such as DM and CVD. It is relevant that dietary components that influence risk of DM, have similar effects on inflammatory biomarkers of cardiovascular risk. Polyphenolic compounds such as flavonoids, isoflavones, phenolic acids and lignan contribute to increased plasma antioxidant capacity, decreased oxidative stress markers and reduced total and LDL cholesterol. They modulate genes associated with metabolism, stress defence, detoxification and transporter proteins. Their antioxidant and anti-inflammatory actions have specific applications for pathologies associated with chronic low-grade systemic inflammation that underpins progression of DM and CVD. Mechanisms involved depend on the structure of the compound, redox status of the inflammatory milieu and other interactions. Bioactive phytochemicals play an important therapeutic role in attenuating oxidative damage induced by metabolic syndrome associated with atherogenic dyslipidaemia and a pro-inflammatory, pro-thrombotic state, at a sub-cellular level. It would be critical to formulate optimal proportions and their combinations for therapeutic efficacy, based on synergistic interactions. Some of these mechanisms and potential actions are discussed.
    Infectious disorders drug targets. 11/2012;
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    ABSTRACT: Periodontal pathogens in plaque biofilm initiate periodontitis, which is influenced by genetic and environmental factors. The resultant pro-oxidant status imposed on the periodontium, exacerbated by episodic hyperinflammatory damage contributes to progression of periodontitis and tooth loss in susceptible subjects. Increasing documentation of bi-directional connections between periodontal and cardiometabolic disorders makes it an intriguing area of therapeutic intervention for mutual benefit. Periodontitis and associated comorbidities demonstrate similar risk markers of inflammation during disease progression. Depending on the extent and severity of the inflammatory response, periodontitis could impact significantly on systemic inflammatory loading and influence the progression of endothelial dysfunction, atherosclerotic plaque instability, dyslipidaemia and insulin resistance. Some of the common mechanisms involved are discussed, relevant to periodontal and cardiometabolic disorders which have been documented as having a bidirectional relationship with periodontal disease progression; abating in response to treatment. Periodontal disease may be a useful marker of a susceptible immune system, or directly affect the progression of systemic diseases due to inflammatory loading. These mechanisms mediated by coordinated actions of cytokines, acute phase proteins, enzymes and their sequelae are addressed in the context of conventional periodontal therapy and its outcome with a modulatory role on metabolic diseases. Applications for the role of nutritional and therapeutic antioxidants as adjuncts in diseases with a distinctly prooxidant profile are discussed. Accurate therapeutic targeting as an adjunct to conventional periodontal treatment in this context, for mutual benefit to subjects with periodontitis and cardiometabolic diseases is a challenge.
    Infectious disorders drug targets. 06/2012; 12(4):301-15.
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    ABSTRACT: The effect of smoking on soft tissues after periodontal treatment has been extensively studied. However, little focus has been placed on the impact of smoking on bone regeneration after treatment. The aim of this review is to systematically assess the effect of smoking on bone regeneration after periodontal treatment. A protocol was established and studies were sourced from five electronic databases. Screening, data abstraction, and quality assessment was conducted by two review authors. Prospective and retrospective clinical studies assessing bone regeneration in smokers and non-smokers after periodontal therapy were selected. In addition, arms of clinical trials comparing different interventions that reported results separately for smokers and non-smokers were also included. Primary outcome measures were based on clinical and/or radiographic indicators of bone regeneration after periodontal therapy. The review and meta-analysis followed many of the recommendations outlined in the preferred reporting items for systematic reviews and meta-analyses statement. Six of 10 studies included in this review concluded that smoking negatively influenced bone regeneration. A meta-analysis of a subgroup of three studies demonstrated that smoking resulted in significantly less bone gain (P = 0.03) as measured by a change in the probing bone level after the treatment of intrabony defects with guided tissue regeneration. The meta-analysis showed a standardized mean difference of -2.05 (95% confidence interval: -2.64 to -1.47) using the random-effects model. Smoking has a negative effect on bone regeneration after periodontal treatment. Patients should be advised that their smoking habit may result in poorer bone regeneration after periodontal treatment.
    Journal of Periodontology 05/2011; 83(2):143-55.
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    ABSTRACT: There is documented evidence of significant associations between cancer of the lung, kidney, pancreas, hematological and oral cancers and periodontal diseases of the supporting structures of the teeth. Enhanced lipid peroxidation, raised levels of TBARS and the oxidative stress marker malondealdehyde have been detected in breast cancer with reduced antioxidant capacity, also characteristic of periodontal diseases. Antioxidants could overcome this deficit and attenuate disease progression by down regulating glutathione detoxification/redox buffering system and inhibiting key transcription factors. Periodontal disease may be a critical marker of a susceptible immune system, or initiate cancer risk with a pro-oxidant inflammatory profile.
    Cancers. 01/2010; 2(2):670-692.
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    ABSTRACT: The aetiopathogenesis of periodontal diseases is initiated by microbial biofilm which could lead to a hyperinflammatory status in aggressive forms of the disease; and cause an imbalance in the redox status, resulting in oxidative stress-induced damage. There is increasing documentation of the link between periodontal and other inflammatory diseases driven by a pro-oxidant profile. This could impose a significant systemic loading of reactive oxygen species relevant to metabolic, arthritic, age related and neoplastic diseases. They demonstrate similar markers of risk / oxidative stress induced injury during disease progression which abate in response to treatment. In certain aggressive forms of periodontal diseases resulting in a substantial systemic pro-oxidant profile, the co-existence of systemic diseases with a similar inflammatory pathogenesis could lead to progressive tissue / organ damage fuelled by the same process. Some of the common mechanisms involved are discussed, relevant to periodontal, metabolic and rheumatoid diseases, pregnancy and the foetus, age related changes and certain neoplasias which have been recently linked to periodontal disease progression. In view of a distinct pro-oxidant profile in severe cases there may a role for selective use of antioxidant adjuncts with suitable therapeutic targeting. It is relevant that periodontal diseases are associated with the above diseases and a small but significant overall cancer risk which persists in non-smokers. Periodontal disease may be a useful marker of a susceptible immune system, or directly affect the progression of systemic diseases due to inflammatory loading. Formulation of therapeutic agents shown to have efficacy in this context, with accurate targeting is a challenge.
    Infectious disorders drug targets. 09/2009; 9(4):415-27.
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    ABSTRACT: Diet and nutrition have played an important role in maintaining physiological homeostasis. Recent literature emphasizes potential therapeutic effects of micronutrients found in natural products, indicating positive applications for controlling the pathogenesis of chronic diseases driven by an inflammatory nidus. Nutritional compounds which display anti-inflammatory and antioxidant effects have specific applications in preventing oxidative stress induced injury which characterizes their pathogenesis. Patient control over diet and disease has been demonstrated in diabetes mellitus, cardiovascular disease, rheumatology, carcinogenesis and other diseases. Polyphenolic compounds are ubiquitous dietary components, mainly flavonoids and tannins. Specific polyphenols are effective in scavenging reactive oxygen and reactive nitrogen species. They are able to modulate genes associated with metabolism, stress defence, drug metabolizing enzymes, detoxification and transporter proteins. Their overall effect is protective in overcoming damaging effects of chronic diseases and in delaying the degenerative effects of ageing. The mechanisms involved in radical scavenging activity are complex, determined by the structure of the compound, redox status of the environment and interactions with other agents. Atherogenic dyslipidaemia associated with a pro-inflammatory pro-thrombotic state in metabolic syndrome and related risk of fatty liver, arthritis, neurodegenerative disorders and certain types of cancers are ideal therapeutic targets for bioactive phytochemicals which can combat oxidative stress induced damage at a sub-cellular level. It is relevant that purified micronutrients isolated from natural products may be less effective than a combination seen in the natural product due to synergistic effects of interacting agents. Some of these mechanisms and potential therapeutic targets are discussed.
    Infectious disorders drug targets. 09/2009; 9(4):400-14.
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    ABSTRACT: The aim of this study was to assess oral health-related beliefs and attitudes, health behaviour of smokers in relation to the Transtheoretical Model (TTM) of behaviour change, willingness to have smoking cessation provided together with periodontal treatment. Postal questionnaire was sent to 500 referred patients. Part 1 looked at attitudes and beliefs about periodontal disease, Part 2 aimed at current smokers focused on the TTM and smoking cessation. Response rate was 56% (n=277); 67% females, 33% males. Mean age was 44.9 years (SD 12.45); 24.5% current smokers, 30.3% past smokers, 45.5% never smokers. Fewer smokers reported "bleeding gums" (p=0.027), but more smokers reported "having loose teeth" (p=0.016). The TTM stages of change indicated that 31% of current smokers were in pre-contemplation of quitting smoking, 46% were in contemplation and 23% were in preparation. Twenty-three percent of the past smokers were in action and 77% in maintenance. Smokers showed differences in the "self-re-evaluation" (p=0.001) and "self-liberation" (p=0.015) processes of change depending on their stage of change (pre-contemplation or preparation). Nearly half (49%) of the current smokers who wanted to quit requested smoking cessation to be provided alongside their periodontal treatment. A large proportion of periodontal patient smokers may be considering quitting, and nearly half requested provision of smoking cessation intervention in conjunction with the periodontal treatment.
    Journal Of Clinical Periodontology 12/2008; 35(11):944-54.
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    ABSTRACT: There are remarkable similarities in the pathogenesis of periodontal diseases and rheumatoid arthritis. The mechanisms that drive antigen induced sequelae of oxidative stress are discussed in this review. A poorly modulated inflammatory response drives both diseases resulting in oxidative stress induced tissue injury. Immune complex formation in response to the periodontal pathogen Porphyromonas gingivalis triggering the production of ROS in both gingivae and synovium of RA patients has been reported. Elevated antibody levels to several periodontal pathogens in RA patients has implications on both RA and periodontal diseases. Periodontal patients are challenged individuals representing a multifactorial aetiopathogenesis with potential for therapeutic intervention in the context of free radical damage. Subjects with moderate to severe periodontal bone loss are significantly more likely than healthy individuals to have several co-existing systemic conditions resulting in ROS mediated damage. There is potential for dual induction of periodontal disease by existing inflammatory mechanisms of systemic diseases rather than exacerbation of low grade inflammation only; emphasizing the relevance of reducing inflammatory burden for disease control. Therapeutic strategies based on disease mechanisms include combined low dose non-steroidal anti-inflammatory drugs and doxycycline for synergistic reduction of matrix metalloproteinase activity in periodontal tissues and RA; sub-optimal dosing with CMT-8 and a biphosphonate clodronate to reduce pathologically elevated levels of MMPs, elastase and to restore alveolar bone in experimental periodontits demonstrating dual applications. Therapeutic interventions relevant to both diseases discussed in this review, have scope for a double hit in periodontal patients with co-existing RA and vice versa.
    Current Drug Metabolism 01/2008; 8(8):750-7.
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    ABSTRACT: Previously we have shown that reference and freshly isolated Treponema denticola cultures possess 5alpha-reductase (5alpha-R) and 3beta- and 17beta-hydroxysteroid dehydrogenase activity. A gene matching the 3-oxo-5alpha-steroid 4-dehydrogenase family protein (gene ID: 2739284; locus tag: TDE2697) has been identified in T. denticola ATCC 35405. The aim of the work presented here was to optimize assay conditions and determine steroid substrate specificities for the 5alpha-R activity of T. denticola ATCC 33520. 5alpha-R activity of cell-free preparations was assayed with radioactive steroid substrates. 5alpha-R-reduced products were identified using thin-layer chromatography and a radioisotope scanner. Assay conditions were optimized for co-factor, buffer and pH requirements. Apparent substrate specificities were determined for progesterone, 4-androstenedione, testosterone and corticosterone. The time-course for metabolism of radiolabelled progesterone and cholesterol substrates was investigated with anaerobic cultures. The optimum pH for 5alpha-R was 5.5 and the preferred co-factor was NADPH. The order of the steroids with respect to their 5alpha-R substrate specificities was (in descending order): progesterone, 4-androstenedione, testosterone and corticosterone. There are at least two intermediates in the synthesis of 5alpha-dihydrocholesterol from cholesterol. These results suggest that the 3-oxo-5alpha-steroid 4-dehydrogenase family protein gene of T. denticola codes for a functional protein that resembles mammalian 5alpha-R isoenzyme 2 with regard to co-factor requirement and pH optimum.
    Oral Microbiology and Immunology 11/2007; 22(5):326-32.
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    ABSTRACT: To investigate patient centred outcomes, soft tissue morphology, and bone levels. Sixty-six subjects, who had completed treatment for a single implant restoration at least l year previously. Appearance was recorded photographically and bone levels and interdental contact points measured from intra-oral radiographs using a x 7 scale loupe. Subjects completed a satisfaction questionnaire. Subjects were highly satisfied with all aspects of the restoration including the appearance of the soft tissue (median shape/colour score 6 on scale 1-6). Twenty-eight sites in 20 subjects had no contact point between implant crown and adjacent tooth. A normal height papilla was judged to be present in 19 of these sites. These were excluded from the subsequent analysis. In the remaining 46 subjects with contact points the presence (JEMT score 3) or deficiency (score 1/2) of the papilla was significantly related to the distance to the bone level on the adjacent tooth and implant head. Differences were observed between the mesial and distal aspects of the implant restoration. Examining clinicians were more critical of the restorations than the patients. The presence of a complete papilla was associated with a slightly greater distance from contact point to bone level than previously reported.
    Journal Of Clinical Periodontology 08/2007; 34(7):633-8.
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