Scielo RSS <![CDATA[South African Dental Journal ]]> http://www.scielo.org.za/rss.php?pid=0011-851620140009&lang=pt vol. 69 num. 9 lang. pt <![CDATA[SciELO Logo]]> http://www.scielo.org.za/img/en/fbpelogp.gif http://www.scielo.org.za <![CDATA[<b>The Board, the Journal... and clods.. (the lump of earth type)!</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900001&lng=pt&nrm=iso&tlng=pt <![CDATA[<b>SADA position statement: dental amalgam</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900002&lng=pt&nrm=iso&tlng=pt <![CDATA[<b>Fifty years of South African Orthodontics celebrated in style!!</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900003&lng=pt&nrm=iso&tlng=pt <![CDATA[<b>Zuleika Nortjé: 25 January 1964 - 15 August 2014</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900004&lng=pt&nrm=iso&tlng=pt <![CDATA[<b>David Anderson: 18 October 1946 - 22 September 2014</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900005&lng=pt&nrm=iso&tlng=pt <![CDATA[<b>Tony Garwood: 6 March 1950 - 1 September 2014</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900006&lng=pt&nrm=iso&tlng=pt <![CDATA[<b>HIV-associated salivary gland enlargement: a clinical review</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900007&lng=pt&nrm=iso&tlng=pt Salivary gland disease is well established as an important HIV associated oral lesion. It manifests as salivary gland swelling involving one or both parotid glands with or without xerostomia. In the context of HIV, the swelling may be due to a wide spectrum of pathological conditions that include reactive or inflammatory disorders, acute and chronic infections, and neoplasms. This paper reviews the epidemiology, pathogenesis, clinical presentation, aspects of diagnosis and management of HIV associated salivary gland enlargement, in particular parotid gland enlargement, due to benign lymphoepithelial cysts (BLEC). Parotid gland enlargement is typically an early manifestation in the HIV-positive patient and should alert healthcare professionals to the likelihood of HIV infection. FNAC of the parotid gland is required to confirm the diagnosis and instituting HAART forms an important part of the management. There is a shift away from surgery in the treatment of this essentially ‘benign’ condition. <![CDATA[<b>Reciprocating instruments in Endodontics: a review of the literature</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900008&lng=pt&nrm=iso&tlng=pt Salivary gland disease is well established as an important HIV associated oral lesion. It manifests as salivary gland swelling involving one or both parotid glands with or without xerostomia. In the context of HIV, the swelling may be due to a wide spectrum of pathological conditions that include reactive or inflammatory disorders, acute and chronic infections, and neoplasms. This paper reviews the epidemiology, pathogenesis, clinical presentation, aspects of diagnosis and management of HIV associated salivary gland enlargement, in particular parotid gland enlargement, due to benign lymphoepithelial cysts (BLEC). Parotid gland enlargement is typically an early manifestation in the HIV-positive patient and should alert healthcare professionals to the likelihood of HIV infection. FNAC of the parotid gland is required to confirm the diagnosis and instituting HAART forms an important part of the management. There is a shift away from surgery in the treatment of this essentially ‘benign’ condition. <![CDATA[<b>The value of three-dimensional imaging in the detection of a case of double pathology in the right maxilla of a patient</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900009&lng=pt&nrm=iso&tlng=pt A 14 year-old Black female was referred for management of an asymptomatic swelling in her right maxilla. The lesion measured 3cm across, was localised lateral to the right ala of the nose, felt bony hard in some areas and soft in others, and was continuous with the maxillary buccal plate. It occupied the right anterior vestibule but there was no palatal expansion. A panoramic radiograph showed a radiopaque lesion surrounded by a radiolucent periphery, but a lack of clarity prompted a computed tomographic scan. The latter revealed two separate lesions, one buccal and one palatal. The buccal lesion showed a well-defined radiolucency containing a radiopaque mass while the palatal lesion showed a small cystic area attached to the neck of an impacted tooth. Differential diagnoses of calcifying odontogenic cyst, adenomatoid odontogenic tumour or ameloblastic fibro-odontoma and dentigerous cyst or odontogenic keratocyst were considered for the two lesions respectively. Enucleation of the buccal lesion and removal of the impacted tooth together with the overlying cyst presented no problem. Histologically the lesions were respectively diagnosed as a calcifying odontogenic cyst and a dentigerous cyst. Histological features are briefly described together with an historical review of the calcifying odontogenic cyst which has evoked much interest and controversy over the past five decades. <![CDATA[<b>Plunging ranula: an unusual multilocular presentation</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900010&lng=pt&nrm=iso&tlng=pt A 32 year-old male patient who was HIV positive presented at the Wits Oral Health Centre complaining of a large swelling of the left submandibular region of three years' duration. The swelling was non-tender, soft and doughy on palpation and appeared to be crossing the midline. Bilateral sub-mandibular and submental lymphadenopathy was present. Intraorally the lesion caused considerable elevation of the floor of the mouth and impaired the flow of saliva. Fluid from the lesion was aspirated and the patient sent for MRI examination. These images revealed a multilocular cystic lesion causing disruption of the mylohyoid muscle. The aspirate consisted of a thick, bloody fluid which tested positive for salivary amylase. A provisional diagnosis of plunging ranula was made. The multilocular nature of the lesion seen on MRI prompted a more extensive surgical approach in order to prevent recurrence. Consequently the sublingual gland was removed via an intraoral approach while the multilocular cyst was dissected by means of a submandibular approach in order to effect complete removal. Microscopic examination of the submitted specimen confirmed the clinical diagnosis of a plunging ranula. <![CDATA[<b>Oral medicine case book 64: some aspects of the pathophysiology of angioedema with special reference to the upper aerodigestive tract</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900011&lng=pt&nrm=iso&tlng=pt Angioedema refers to a localized oedematous swelling of subcutaneous or sub-mucosal tissues, caused by dilatation and increased permeability of blood vessels, usually mediated either by histamine or by bradykinin. Deficiency or loss of functional activity of the complement component C1 esterase inhibitor (C1-INH) affects multiple systems, including the kallikrein-kinin, complement, coagulation and fibrinolytic pathways, and in the context of angioedema, the result is increased production and release of bradykinin and other vasoactive substances such as C3a. Owing to impairment of C1-INH, factors XIIa and kallikrein, by a positive feedback mechanism, bring about persistent activation of the kallikrein-kinin pathway with amplification of production of bradykinin, resulting in angioedema. Histamine can cause histaminergic angioedema. As the name implies, this oedema is caused by degranulation of mast cells/ basophils as a result of an IgE-dependant allergic reaction to extracts of food, drugs, infectious agents, or to physical stimulation; or as the result of direct degranulation of mast cells/basophils independently of IgE, caused by releasing agents such as opiates, antibiotics or radio-contrast media. As dental, oral and maxillofacial operative procedures may trigger the development of angioedema in susceptible individuals, the dental practitioner should be familiar with its signs and symptoms, its pathophysiology and with the firstline treatment of this disorder. <![CDATA[<b>Maxillo-facial radiology case 125</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900012&lng=pt&nrm=iso&tlng=pt Angioedema refers to a localized oedematous swelling of subcutaneous or sub-mucosal tissues, caused by dilatation and increased permeability of blood vessels, usually mediated either by histamine or by bradykinin. Deficiency or loss of functional activity of the complement component C1 esterase inhibitor (C1-INH) affects multiple systems, including the kallikrein-kinin, complement, coagulation and fibrinolytic pathways, and in the context of angioedema, the result is increased production and release of bradykinin and other vasoactive substances such as C3a. Owing to impairment of C1-INH, factors XIIa and kallikrein, by a positive feedback mechanism, bring about persistent activation of the kallikrein-kinin pathway with amplification of production of bradykinin, resulting in angioedema. Histamine can cause histaminergic angioedema. As the name implies, this oedema is caused by degranulation of mast cells/ basophils as a result of an IgE-dependant allergic reaction to extracts of food, drugs, infectious agents, or to physical stimulation; or as the result of direct degranulation of mast cells/basophils independently of IgE, caused by releasing agents such as opiates, antibiotics or radio-contrast media. As dental, oral and maxillofacial operative procedures may trigger the development of angioedema in susceptible individuals, the dental practitioner should be familiar with its signs and symptoms, its pathophysiology and with the firstline treatment of this disorder. <![CDATA[<b>Transcultural and language barriers to patient care</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900013&lng=pt&nrm=iso&tlng=pt Angioedema refers to a localized oedematous swelling of subcutaneous or sub-mucosal tissues, caused by dilatation and increased permeability of blood vessels, usually mediated either by histamine or by bradykinin. Deficiency or loss of functional activity of the complement component C1 esterase inhibitor (C1-INH) affects multiple systems, including the kallikrein-kinin, complement, coagulation and fibrinolytic pathways, and in the context of angioedema, the result is increased production and release of bradykinin and other vasoactive substances such as C3a. Owing to impairment of C1-INH, factors XIIa and kallikrein, by a positive feedback mechanism, bring about persistent activation of the kallikrein-kinin pathway with amplification of production of bradykinin, resulting in angioedema. Histamine can cause histaminergic angioedema. As the name implies, this oedema is caused by degranulation of mast cells/ basophils as a result of an IgE-dependant allergic reaction to extracts of food, drugs, infectious agents, or to physical stimulation; or as the result of direct degranulation of mast cells/basophils independently of IgE, caused by releasing agents such as opiates, antibiotics or radio-contrast media. As dental, oral and maxillofacial operative procedures may trigger the development of angioedema in susceptible individuals, the dental practitioner should be familiar with its signs and symptoms, its pathophysiology and with the firstline treatment of this disorder. <![CDATA[<b>What's new for the clinician? Summaries of and excerpts from recently published papers</b>]]> http://www.scielo.org.za/scielo.php?script=sci_arttext&pid=S0011-85162014000900014&lng=pt&nrm=iso&tlng=pt Angioedema refers to a localized oedematous swelling of subcutaneous or sub-mucosal tissues, caused by dilatation and increased permeability of blood vessels, usually mediated either by histamine or by bradykinin. Deficiency or loss of functional activity of the complement component C1 esterase inhibitor (C1-INH) affects multiple systems, including the kallikrein-kinin, complement, coagulation and fibrinolytic pathways, and in the context of angioedema, the result is increased production and release of bradykinin and other vasoactive substances such as C3a. Owing to impairment of C1-INH, factors XIIa and kallikrein, by a positive feedback mechanism, bring about persistent activation of the kallikrein-kinin pathway with amplification of production of bradykinin, resulting in angioedema. Histamine can cause histaminergic angioedema. As the name implies, this oedema is caused by degranulation of mast cells/ basophils as a result of an IgE-dependant allergic reaction to extracts of food, drugs, infectious agents, or to physical stimulation; or as the result of direct degranulation of mast cells/basophils independently of IgE, caused by releasing agents such as opiates, antibiotics or radio-contrast media. As dental, oral and maxillofacial operative procedures may trigger the development of angioedema in susceptible individuals, the dental practitioner should be familiar with its signs and symptoms, its pathophysiology and with the firstline treatment of this disorder.