Abstract
AIM: To evaluate the manifestations of sickle cell disease on the orofacial complex through a review of current literature concerning prevalence of dental caries, periodontal disease, temporomandibular joint disorders and radiographic alterations of maxillofacial bones. METHODS: Full-text papers retrieved from MEDLINE and LILACS electronic databases were critically reviewed. RESULTS: Alterations of maxillofacial bones are well documented in the literature, but studies reporting caries, periodontal condition and temporomandibular joint alterations in are scarce and inconclusive. CONCLUSION: Further well-designed epidemiological studies are needed to indicate the real impact of this disease on the stomatognathic health, collaborating to improve public health policies.
Highlights
IntroductionSickle cell disease (SCD) includes genetic blood disorders in which morphologic alterations of erythrocytes are caused by presence of the sickle hemoglobin (HbS)
Received for publication: May 07, 2013 Accepted: September 17, 2013Sickle cell disease (SCD) includes genetic blood disorders in which morphologic alterations of erythrocytes are caused by presence of the sickle hemoglobin (HbS)
SCD can be found in several countries affecting people all over the world, but primarily affects African descendents[5]
Summary
Sickle cell disease (SCD) includes genetic blood disorders in which morphologic alterations of erythrocytes are caused by presence of the sickle hemoglobin (HbS). The heterozygosis for genes of normal (HbA) and mutant (HbS) hemoglobins (AS genotype) does not exhibit clinical symptoms of the disease under physiological conditions[3,5]. Several other complications have been described, including: stroke, pulmonary infarct with decreased lung function, priapism, chronic renal failure, splenic and hepatic dysfunctions, jaundice, retinal ischemia causing transient or permanent blindness, chronic leg ulceration, apathy, cardiac alterations, convulsion and osseous alterations like osteonecrosis, osteomyelitis, osteopenia and osteoporosis[4,10,11] It is noted a wide interindividual variety of disease severity that has been suggested as result of polymorphisms in several genes[12], mainly of fetal hemoglobin which has been pointed as a target for promising treatments[13].
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