Kaposi’s sarcoma (KS) is a tumor caused by Human herpesvirus 8 (HHV8), also known as Kaposi’s sarcoma-associated herpesvirus (KSHV). It was originally described by Moritz Kaposi (KA-po-she), a Hungarian dermatologist practicing at the University of Vienna in 1872. It became more widely known as one of the AIDS defining illnesses in the 1980s. The viral cause for this cancer was discovered in 1994. Although KS is now well-established to be caused by a virus infection, there is widespread lack of awareness of this even among persons at risk for KSHV/HHV-8 infection. Continue reading
Category Archives: Oral medicine
Progeria Part 2
A type of anticancer drug, the farnesyltransferase inhibitors (FTIs), has been proposed, but their use has been mostly limited to animal models. A Phase II clinical trial using the FTI lonafarnib began in May 2007. In studies on the cells another anti-cancer drug, rapamycin, caused removal of progerin from the nuclear membrane through autophagy. It has been proved that pravastatin and zoledronate are effective drugs when it comes to the blocking of farnesyl group production. However, it is important to remember that no treatment is able to cure progeria. Continue reading
Progeria Part 1
Progeria (also known as “Hutchinson–Gilford Progeria Syndrome“, “Hutchinson–Gilford syndrome“, and “Progeria syndrome“) is an extremely rare genetic condition wherein symptoms resembling aspects of aging are manifested at an early age. The word progeria comes from the Greek words “pro” (Ï€ÏÏŒ), meaning “before”, and “géras” (γῆÏας), meaning “old age”. The disorder has very low incidences and occurs in an estimated 1 per 8 million live births. Those born with progeria typically live to their mid teens and early twenties. It is a genetic condition that occurs as a new mutation (de novo), and is rarely inherited. Although the term progeria applies strictly speaking to all diseases characterized by premature aging symptoms, and is often used as such, it is often applied specifically in reference to Hutchinson-Gilford Progeria Syndrome (HGPS). Continue reading
Hurler’s Syndrome
Hurler syndrome, also known as mucopolysaccharidosis type I (MPS I), Hurler’s disease, also gargoylism, is a genetic disorder that results in the buildup of glycosaminoglycans (formerly known as mucopolysaccharides) due to a deficiency of alpha-L iduronidase, an enzyme responsible for the degradation of mucopolysaccharides in lysosomes. Without this enzyme, a buildup of heparan sulfate and dermatan sulfate occurs in the body. Symptoms appear during childhood and early death can occur due to organ damage. Continue reading
Chediak-Higashi syndrome
Chédiak–Higashi syndrome is a rare autosomal recessive disorder that arises from a microtubule polymerization defect which leads to a decrease in phagocytosis. The decrease in phagocytosis results in recurrent pyogenic infections, partial albinism and peripheral neuropathy. It occurs in humans, cattle, white tigers, blue Persian cats, Australian blue rats, mice, mink, foxes, and the only known captive albino orca. Continue reading
Apert syndrome Part 2
Causes
Acrocephalosyndactyly may be an autosomal dominant disorder. Males and females are affected equally; however research is yet to determine an exact cause. Nonetheless, almost all cases are sporadic, signifying fresh mutations or environmental insult to the genome. The offspring of a parent with Apert syndrome has a 50% chance of inheriting the condition. In 1995, A.O.M. Wilkie published a paper showing evidence that acrocephalosyndactyly is caused by a defect on the fibroblast growth factor receptor 2 gene, on chromosome 10. Continue reading
Apert syndrome Part 1
Apert syndrome is a form of acrocephalosyndactyly, a congenital disorder characterized by malformations of the skull, face, hands and feet. It is classified as a branchial arch syndrome, affecting the first branchial (or pharyngeal) arch, the precursor of the maxilla and mandible. Disturbances in the development of the branchial arches in fetal development create lasting and widespread effects. Continue reading
Anatomy of temporomandibular joint Part 3
The disc is thick all around its rim, and thin in the centre. From anterior to posterior it shows – anterior extension, thick anterior band (2.0mm thick), intermediate thin zone (1.0 mm thick), thick posterior band (3.0 mm thick) and posterior most bilaminar region (Dubrul, 1996; Williams et al, 1999). The disc is attached all around the joint capsule except the strong straps those fix the disc directly to the medial and lateral condylar poles which ensures that the disc and condyle move together in protraction and retraction (Choukas and Sicher, 1960; Williams et al, 1999). The anterior extension of the disc is attached to fibrous capsule superiorly and inferiorly and through that to temporal bone and the mandibular neck respectively. In between it gives insertion to lateral pterygoid muscle where the fibrous capsule is lacking and synovial membrane is supported only by loose areolar tissue. In the opinion of Kreutziger and Mahan (1975), this deficiency anteriorly is the weak point since there is no fibrous resistance to hypertranslation. Apart from lateral pterygoid, anteromedially, there are attached some fibres of masseter and temporalis laterally. Although more than one muscle is inserted into the disc, majority of the interest has been focussed on lateral pterygoid, whose deep position, unfortunately makes it difficult to investigate under natural conditions (Moore). Continue reading
Anatomy of temporomandibular joint Part 2
Articular coverings :
The smooth slippery, pressure bearing tissue carpeting, the surfaces of the bones varies in thickness across different articular areas. It is essentially a bed of tough collagen fibres bound by special glycoproteins. On the condyle, the tissue is thickest in anteroposterior direction and thickness is greater medially (average measurements 0.37 mm laterally and 0.48 mm medially). On temporal component, it is thickest along articular eminence and preglenoid plane. The thickness is less medially (0.49 mm and 0.36 mm for eminence and plane respectively laterally and 0.45 mm and 0.34 mm medially). In the depth of the mandibular fossa the thickness of periosteum is merely 0.07 mm. Continue reading
Anatomy of Temporomandibular Joint Part 1
Temporomandibular joint also known as jaw joint or mandibular joint is an ellipsoid variety of synovial joints, right and left joints forming a bicondylar articulation (Williams et al, 1999). The common features of synovial joints exhibited by this joint include a fibrous capsule, synovial membrane et fluid and tough adjacent ligaments etc. However the features which differentiate and make it unique in itself are: Continue reading