Ethical and legal issues around HIV/AIDS in dentistry in South Africa.
Explore the source record for details and available documents.
AIDS Serodiagnosis↗
Biomedical subjects
S Naidoo
Publications and source records attributed to S Naidoo.
Hypohydrotic ectodermal dysplasia: an unusual presentation and management in an 11-year-old Xhosa boy.
Ectodermal dysplasia (ED) is an inherited disorder in which two or more ectodermally derived structures fail to develop, or are abnormal in development. Hypohydrotic ectodermal dysplasia (HED) or Christ-Siemens-Touraine syndrome, is an X-linked recessive syndrome with an incidence of 1/10,000 to 1/100,000 births. Because of its X-linked inheritance pattern, it is more common in males. HED is characterised by hypohydrosis (diminished perspiration), hypotrichosis (decreased amount of hair) and microdontia (small teeth), hypodontia (lack of development of one or more teeth) or adontia (total lack of tooth development). These patients present diagnostic and treatment challenges because of variable oral manifestations. This report describes an 11-year-old Xhosa boy, who was referred to the University Dental Faculty by his general medical practitioner because of hypodontia. General facial features included: frontal bossing, a depressed nasal bridge, 'butterfly' pattern of eczema over the nasal bridge to the malar process of each cheek, thinned out hair, loss of vertical dimension of face and dry skin. Intra-oral examination revealed hypodontia with peg-shaped anterior teeth and diastemas. Radiological examination revealed no developing permanent teeth or tooth buds. Diagnosis was confirmed by doing a sweat gland count. Management included oral hygiene instruction, fluoride treatments, construction of a partial lower denture and counselling about his condition with particular reference to the danger of hyperthermia and control of allergies.
Anodontia↗
Tissue kallikrein and kinins in renal disease.
The renal kallikrein-kinin system is involved in sodium and water homeostasis, blood pressure regulation and inflammation. Tissue kallikrein and kinin levels were measured in the urine of patients with renal disease and in the urine of living related kidney donors prior to uninephrectomy who served as controls. Tissue kallikrein and kinin B1 and B2 receptors were immunolocalised by confocal microscopy in renal biopsy material from patients with renal disease and controls (fresh autopsy material and normal kidney tissue from nephrectomies for malignancy). Urinary tissue kallikrein excretion was significantly decreased in patients with mild renal disease (16.6 +/- 6.7 ng tissue kallikrein (TK)/ng protein; p < 0.05) and more markedly so (1.8 +/- 0.7 ng TK/microg protein; p < 0.01) in patients with severe renal failure requiring dialysis compared to normal controls (78.9 +/- 31.7 ng TK/microg protein). Basal kinin values were unchanged in patients with renal disease (14 +/- 0.8 ng/ml) compared to controls (13.3 +/- 0.56 ng/ml). In control kidney tissue kallikrein was immunolocalised in the distal connecting tubules and collecting ducts whereas decreased immunolabelling was observed with renal disease. Kinin B2 receptor labelling was present in the entire nephron in the normal control kidney but was reduced with renal disease. While kinin B1 receptor immunolabelling was not observed in the control kidneys, labelling of distal tubules and collecting ducts was noted in renal disease, suggesting an upregulation of B1 receptors in renal parenchymal disease.
Adolescent↗
Endothelin-1 and endothelin receptor status in kidney transplants undergoing acute rejection.
Endothelin-1 (ET-1) is a potent vasoconstrictor with vasopressor and mitogenic effects. Blood samples were collected from 21 renal transplant patients undergoing acute rejection at the time of diagnostic kidney biopsy: there were 20 men and one woman, mean age 35.6 years. All patients were on triple immunosuppressive therapy with cyclosporine A, azathioprine and methylprednisolone. Twenty living kidney donors pre-uninephrectomy (11 men and nine women, mean age 34 years) served as controls. Control kidney was obtained from fresh autopsy material and normal kidney tissue from nephrectomies for malignancy. Mean plasma ET-1 was significantly increased at 1.56 +/- 0.2 pg ml(-1) during acute rejection compared to 0.74 +/- 0.06 pg ml(-1) in donors (p = 0.0009 unpaired t-test). ET(A) receptor immunolabelling was visualised in distal tubules and collecting ducts with minimal labelling in the glomeruli and blood vessels of control kidney tissue ET(A) receptor labelling was similar in kidney biopsies with acute rejection. ET(B) receptor immunolabelling was significantly increased in glomeruli (p = 0.002) and decreased in distal tubules (p = 0.004) in kidneys with acute rejection compared to control kidney tissue. While these findings may account for the oedema and hypertension observed during acute rejection, the exact significance needs to be studied further.
Acute Disease↗
Correlation of kinin generating activity with Helicobacter pylori-associated gastric infection.
The kallikrein-kinin system involves a biologically complex set of interactive proteases that signal the first-line onset of inflammation and associated cellular processes. The basic enzymatic cleavage of kininogen substrate by the serine protease tissue kallikrein to liberate kinins is regulated by a number of factors. These may include the recently discovered bacterial involvement in the causation of gastritis. The gram-negative Helicobacter pylori organism, colonises the human gastric epithelium and initiates ulcerogenesis and may induce, in the longer term, tumour formation. The aim of this study was to investigate the role of kinins in H. pylori-induced gastric dyspepsia. During endoscopic examination, lavage aspirates of 23 patients were collected, and the tissue kallikrein content measured by a kinin-generating assay and an enzyme-linked immunosorbent assay. Gastric antral and pyloric biopsy tissue was histologically examined for degrees of inflammation and H. pylori infection, and then immunolabelled for tissue kallikrein and kinin receptors. Results show that labelled tissue kallikrein in the fundic glands and parietal cells of the diseased antrum was elevated with increasing severity of gastritis. Further, kinin-generating potential of the lavage fluid appeared to be greater with increasing evidence of infection. Tissue kallikrein immunosorbent assay levels were significantly raised in patients showing mild to moderate H. pylori infection. One outcome of this study may be the inclusion of kinin antagonists in management of gastric dyspepsia.
Adolescent↗
Identification of immunoreactive tissue prokallikrein on the surface membrane of human neutrophils.
Putative binding sites for prokallikrein, the endogenous zymogen of the vasoactive and pro-inflammatory tissue kallikrein-kinin system, were recently demonstrated on human neutrophils. However, the occurrence and distribution of neutrophil-bound prokallikrein itself have so far not been examined. In this study, a specific anti-peptide antibody directed against the propart of the zymogen was used to localize the kallikrein precursor by confocal laser-scanning microscopy on unstimulated human blood neutrophils. Our results describe, for the first time, the presence of tissue prokallikrein on the membrane of circulating neutrophils. Immunoreactive prokallikrein was associated into punctate clusters occupying the external surface of the neutrophil membrane and, after addition of exogenous zymogen, immunolabeling was enhanced four-fold. In contrast, only moderate immunoreactivity to prokallikrein was observed intracellularly. These results suggest that resting neutrophils provide a circulating platform for tissue prokallikrein whose surface density may be upregulated as part of the inflammatory process.
Cell Membrane↗
Urinary tissue kallikrein excretion in black African women with severe pre-eclampsia.
BACKGROUND: A study of tissue kallikrein excretion in African women with severe pre-eclampsia. METHODS: Random untimed urine samples were collected from all women (n=198) recruited to this study; 66 women with severe pre-eclampsia, 66 normotensive pregnant women of similar length of gestation and 66 normotensive non-pregnant women. Urine specimens were analyzed for urinary tissue kallikrein using a selective, synthetic chromogenic tripeptide substrate (S2266) having the sequence H-D-Val-Leu-Arg-pNA. RESULTS: Urinary tissue kallikrein levels were decreased in women with severe pre-eclampsia compared with those of gestation matched normotensive pregnant women at 28 weeks of gestation (1.55+/-0.95 vs. 3.02+/-1.35 ng TK/microg protein; p<0.0001) and at near delivery date (1.21+/-0.53 vis. 3.11+/-1.2 ng TK/microg protein; p<0.0001). In the normotensive pregnant group, there was no significance difference in urinary tissue kallikrein excretion close at delivery date compared to 28 weeks of gestation (3.02+/-1.35 vs. 3.11+/-1.21 ngTK/microg protein; p=0.23). No statistical difference in urinary tissue kallikrein excretion was observed between normotensive pregnant and normotensive non pregnant women (3.02+/-1.35 vs. 2.97+/-1.12 ngTK/microg protein; p=0.16). Urinary tissue kallikrein excretion correlated positively with urinary creatinine levels at 28 weeks of gestation (r=0.69; p<0.0001) and close to delivery date (r=0.84; p<0.0001). There was no correlation between neonatal birthweight and urinary tissue kallikrein levels (r=-0.44; p=0.41). CONCLUSION: The decreased levels of urinary tissue kallikrein excretion in pre-eclamptic patients suggests an etiological role for this serine protease in hypertensive disorders of pregnancy.
Adult↗
HIV/AIDS - the evolving pandemic and its impact on oral health in sub-Saharan Africa.
This review provides an update on HIV/AIDS based on a literature search (1989-1999) in respect of its epidemiology and oral manifestations in sub-Saharan Africa. The African epidemic is unique in its heterosexual spread, high prevalence in men, women and children, rapid rise in young women and risk of vertical transmission. Viral subtypes A and D predominate in Africa, subtype C in South Africa and subtype E in Central Africa. The pandemic is fueled by endemic poverty, malnutrition, gender inequality and sexual and cultural practices. Oral lesions may frequently be the initial presenting signs of HIV infection, early clinical features, predictors of progression of disease and may be useful in staging and classification. Health care workers require training to understand, diagnose, manage and research these manifestations.
AIDS-Related Opportunistic Infections↗
Immunolocalization of bradykinin receptors on human synovial tissue.
Kinins have been implicated in the pathogenesis of experimental and clinical inflammatory arthritis. Previous studies have reported increased amounts of plasma and tissue kallikreins in synovial fluid, raised kinin levels and an upregulation of kinin B2 receptors on synovial fluid neutrophils in rheumatoid arthritis. Bradykinin binding sites have been identified on human synovial cells by autoradiographic localization and Scatchard analysis. This study was undertaken to localize immunohistochemically kinin B1 and B2 receptors on human synovial tissue. Synovial tissue was obtained at the time of joint replacement surgery or arthroscopic synovectomy in six patients (two RA, two OA and two with avascular necrosis). Tissue sections were immunolabelled for kinin B1 and B2 receptors and viewed by light and confocal microscopy. No immunolabelling of the kinin receptors was observed in the method controls. In all patients labelling for kinin B2 receptors was observed in the synovial lining cells, fibroblasts and endothelial lining cells of blood vessels. There was no immunolabelling for kinin B1 receptors in all samples. These findings further support a role for the B2 receptors in joint diseases. There did not appear to be an induction of the kinin B1 receptor in human synovial tissue obtained from patients with chronic arthritis. However, further studies are required to assess the role of B1 receptors in active joint inflammation.
Animals↗
Kinin receptors in human vascular tissue: their role in atheromatous disease.
Using samples of many human blood vessels, obtained at autopsy and specific antibodies directed to peptide sequences of the kinin B1 and B2 receptors, we demonstrate the localisation of these receptors within the human vascular system using standard immunolabelling techniques. In large elastic arteries and veins, kinin receptors are present only in the endothelial cells whereas in all muscular arteries and arterioles, these receptors are present in both the endothelial and smooth muscle cells. The identification of kinin receptors in human blood vessels confirms that kinins may modulate both vascular permeability and contractility. The incidental finding at histology, of patchy atheromatous disease in the coronary, femoral, vertebral and pericallosal arteries, assisted in elucidating the role of these receptors in the commonest disease affecting human blood vessels. Intense labelling for B1 receptors was observed in the endothelial cells, foamy macrophages, inflammatory cells and fibroblasts within the thickened intima of the plaque as well as in smooth muscle cells of the underlying tunica media. Immunoreactive B2 receptors were also observed in these cells but with reduced intensity. The intense immunolabelling of B1 receptors in these regions suggest that these may be induced by atheromatous disease and may have therapeutic importance for the B1 receptor antagonists.
Amino Acid Sequence↗
Kinin receptor status in normal and inflammed gastric mucosa.
No documented studies have been reported on the presence of B1 and B2 kinin receptors in the mammalian gastric mucosa. This first study aimed to immunolocalise sites of B1 and B2 kinin receptors in the human pyloric gastric mucosa and to evaluate its role in gastritis. Biopsies were obtained from patients with dyspepsia during endoscopic examination of the patient. The diagnosis and grading of the gastritis was performed on histological examination. Sections were immunostained for both B1 and B2 receptors using rabbit anti-human B1 and B2 kinin receptor antibodies. Control tissue was obtained from partial gastrectomy specimens, following surgical excision of the antrum for duodenal ulcers. The control antrum tissue showed strong immunoreactivity for kinin B2 receptors with positivity noted along the luminal border, at the base of the mucous and stem cells. The B1 receptor was not immunolocalised. Biopsies of all five patients with gastritis showed a decrease in immunolabelling of the B2 receptor and an induction of the B1 receptor especially in regenerating cells. In gastritis there is destruction of the normal mucosal glandular architecture with subsequent regeneration of the epithelial cells. The pyloric glands are infiltrated by acute inflammatory cells that cause crypt abscesses with loss of the epithelial cell membranes. This may explain the reduction in the immunolocalisation of the B2 kinin receptors and the induction of the B1 receptors in active gastritis. Follow up studies after treatment of the inflammation with a combination of B1/B2 kinin receptor antagonists are indicated.
Adult↗
Changes in urinary tissue kallikrein excretion in black African women with hypertensive disorders of pregnancy.
The aim of this study was firstly to establish whether tissue kallikrein (TK) was involved in the aetiology of hypertensive disorders of pregnancy. Secondly, to assess whether tissue kallikrein:creatinine ratios may differentiate normotensive pregnant women from those with hypertensive disorders of pregnancy and have a predictive value. Random untimed urine samples were collected from all women (n = 264) recruited to this study. Urine specimens were analyzed for urinary tissue kallikrein using a selective, synthetic chromogenic tripeptide substrate (H-D-Val-Leu-Arg-pNA). Urinary creatinine levels were measured using standard methods. There was a significant difference in the excretion of urinary tissue kallikrein between normotensive pregnant women (2.91 ng TK/microgram protein) and women with mild (2.52 ng TK/microgram protein; p < 0.0001) and severe (1.53 ng TK/microgram protein; p < 0.0001) hypertension in pregnancy. No statistical difference was observed with regard to urinary tissue kallikrein excretion between normotensive pregnant and normotensive non-pregnant women (2.87 ng TK/microgram protein; p = 0.16). A positive correlation was observed between the diastolic blood pressure and urinary tissue kallikrein excretion in women with hypertensive disorders of pregnancy. When compared to the normotensive pregnant group, the urinary kallikrein:creatinine ratios were significantly lower in the mild (0.6 versus 0.3; p < 0.0001) and severe (0.6 versus 0.12; p < 0.0001) hypertensive groups. The urinary creatinine excretion was significantly higher in the mild (9.55 +/- 2.6 mmol/l; p < 0.0001) and in severe (15.62 +/- 5.48 mmol/l; p < 0.0001) hypertensives when compared to normotensive pregnant values (5.65 +/- 2.6 mmol/l). The reduced urinary tissue kallikrein excretion in hypertensive disorders of pregnancy may be a significant factor in the development of the hypertension in pregnancy. Measurement of urinary tissue kallikrein: creatinine ratios may represent a simple and practical predictive test to differentiate women with hypertensive disorders of pregnancy from normotensive pregnant women.
Adult↗
Tissue kallikrein in transplant kidney.
Literature survey, thus far, has shown a decrease in the excretion of urinary tissue kallikrein (TK) in transplant patients with a further reduction of the enzyme during episodes of acute rejection. The study aims were to compare, at cellular and subcellular levels, the localisation of tissue kallikrein in biopsies of the transplant kidney to autopsy derived normal renal tissue. Renal biopsies from eighteen transplant patients with deteriorating renal function were obtained. Immunolabelling for tissue kallikrein, using a polyclonal goat anti-TK, antibody raised against recombinant TK, was performed following routine enzymatic, immunofluorescence and electron microscopic techniques. In normal kidney tissue, TK was immunolocalised in the distal connecting tubules and collecting ducts. By comparison the renal transplant tissue showed a reduction in the intensity of label, but maintained the sites of localisation. In the sections examined by electron microscopy, although TK was confined mainly at the luminal side of the cell, some label was noted along the basolateral membranes. In the transplant kidneys, there was a reduction in the overall number of gold particles counted, which correlated with the decreased intensity observed on immunocytochemistry. In addition, there was a shift to a basolateral orientation of the immunolabel. Acute rejection is characterised by oedema, tubulitis and vasculitis. Destruction of the tubule cells and leakage of TK into the interstitial tissue space and the resultant effect of the formed kinins on renal capillary vasculature could explain the observed renal parenchymal oedema and transplant rejection.
Adult↗
The evaluation of tissue kallikrein in Helicobacter pylori-associated gastric ulcer disease.
Helicobacter pylori (Hp) associated ulcer disease is a common form of gastric disorder involving mucosal damage and invasion of the mucosa by polymorphic inflammatory cells with concomitant changes in the epithelial cell structure. The bacteria are thought to adhere by specific junction zones to the epithelial cell surface resulting in the degeneration of the mucosal layer. Our study was undertaken to examine the relative status of tissue kallikrein (TK) in antral and fundic biopsies, endoscopically obtained from 10 patients suspected of having gastric disorders. For histological evidence of inflammation the tissue was stained with hematoxylin and eosin and classified as mild, active, chronic and chronic active gastritis. Hp infection was determined by Giemsa staining. For localisation of TK, slide-mounted tissue sections were subjected to PAP and immunofluorescent staining using a goat anti-human TK IgG antibody. The results revealed that in the antral control tissue, removed during partial antractomy, TK was immunovisualised along the luminal border of the deep pyloric glands. The surface epithelia and superficial glands showed no labelling. The fundic control tissue revealed an absence of TK in the superficial and surface epithelial glands, but was positive in the parietal cells. The fundic biopsy specimens showed similar immunoreactivity in these areas. By contrast, in the inflammed pyloric mucosa, there was a shift of TK localisation to the basal part of the glandular cells and there was also expression of TK in the superficial glands that showed histological evidence of regeneration. In the fundic biopsies there was no change observed in the sites of TK localisation (similar to control tissue). It was observed, that even though 8 of the 10 subjects exhibited Hp infection, the inflamed mucosa showed no discernable difference in the staining patterns between the infected and non-infected tissue sections. Our findings suggest an important role for a B1/B2 kinin antagonist in patients with gastritis.
Adolescent↗
Dental practitioner risk, knowledge and practice with regard to the hepatitis B vaccination in South Africa.
OBJECTIVES: To determine dental practitioner risk, knowledge and practice with regard to hepatitis B vaccination in South Africa. DESIGN: Cross-sectional, descriptive study. SUBJECTS: Dental students qualifying from the University of the Western Cape dental school between 1985 and 1995 (n = 173). METHODS: A telephonic survey, using a structured questionnaire. MAIN OUTCOME MEASURES: Knowledge and compliance with hepatitis B vaccination. RESULTS: The present study shows that (i) individuals are not maintaining HBV protection and (ii) individuals are at risk. CONCLUSIONS: Guidelines need to be developed to ensure that the entire dental team is not only vaccinated against HBV, but that post-vaccination testing and follow-up for booster vaccination is strictly adhered to.
Adult↗
What are you doing about child abuse?
The Prevention of Family Violence Act, No 33 of 1993, Section 4 read with section 6, makes it an offence for any person who examines, treats, attends to, advises, instructs or cares for any child not to report any suspicion of abuse to a police official, social worker or Commissioner of Child Welfare. If found guilty, the sentence is a fine, or imprisonment up to three months. In terms of Section 42 of the Child Care Act No 74 of 1983, a dentist, medical practitioner, nurse or social worker who deals with a child, commits an offence if suspected child abuse is not reported to the Director General, Welfare or any officer designated by the latter. If found guilty, the sentence is a R4 000 fine or imprisonment for one year.
Child↗
Dentists and cross-infection.
A structured questionnaire was administered to a random sample of general dental practitioners in Natal, South Africa in 1994, to ascertain the precautions they use against cross-infection and to gauge the attitudes and behaviour towards the treatment of HIV-infected individuals. An interview was conducted covering 5 broad topics: demographic details, personal barrier protection, instrument sterilization and disinfection, sharps disposal and incidence of needlestick injuries and the extent of the knowledge, attitude and behaviour of the practitioners toward the treatment of HIV-infected individuals. The key findings were: routine glove wearing, for all patients, was practised by 87 per cent. The most common heat sterilization method was by autoclave (68 per cent), although a dry heat sterilizer and water boiler were used by 22 per cent of the respondents. Of the 18 respondents reporting a needlestick injury in the past 6 months only one sought after-care. 42 per cent of the respondents would continue to treat carriers of HIV in their practices. This survey shows that a significant number of dentists are using unacceptable cross-infection control procedures. Educational efforts should be made to improve their knowledge and to alleviate anxiety of health workers to treat HIV-infected patients.
Adult↗
Regional distribution of tissue kallikrein in the human brain.
Except for the localisation of tissue kallikrein (TK) in human prolactin secreting adenomas, its apparent deficiency in Alzheimer's disease and presence in human cerebrospinal fluid (CSF), the regional distribution of TK in human brain has not been defined. In this study on human brains collected within 24 h of death, we report on the regional distribution of TK in 24 different brain areas. The presence of TK was determined by its amidase and kininogenase activities, and the cellular localisation by immunocytochemistry. The highest amidolytic activity using the substrate D-ValLeuArg-pNA was recorded with extracts of the choroid plexus and hypothalamus, whereas extracts of the cerebral cortex (5 areas), cerebellum (3 areas), brain stem and thalamus possessed moderate amidolytic activity which correlated with the kininogenase assay. Immunoreactive TK has thus far been visualised in neurones of the hypothalamus, thalamus and reticular areas of the brain stem, as well as in cells of the anterior pituitary and choroid plexus by light and confocal microscopy. The cellular distribution of TK in specific areas suggests a role for TK in the neurones and epithelial cells of the brain. The question whether the functional importance of TK may relate to a particular cell type remains to be elucidated.
Brain Chemistry↗