Out of the 500 images taken, 60 children had at least one or more missing permanent teeth. The results showed that more females had one or more missing permanent teeth than males. From the 60 children who had missing permanent teeth, 15.5% were female and 8.8% were males.A case study conducted in 2016 of a 6 year old boy presented with anodontia. There was no family history of anodontia and the patient did not present any other symptoms for ectodermal dysplasia. It was observed the hypodontia was present in the maxillary arch and the only teeth present were the left primary first molar and the bilateral primary second molars. It was also observed that the buccal mucosa, palate, and floor of the mouth were considered normal. The patient proceeded with oral rehabilitation and give removable denture to wear. The patient struggled in the beginning to keep wearing the denture until gradually learning to adjust to it. The family reported no problems with retention and began a monthly recall visit in order to monitor any eruptions of teeth or adjustments that needed to be made. Improvements in speech skills, communication, and self esteem were also observed after placement of the denture.Another case study in 2013 of an eight year old boy who reported missing teeth, difficulty chewing, and difficulty speaking was seen to have other symptoms of ectodermal dysplasia. The father confirmed there is a family history of missing teeth.
That is, instead of being collected at the end of its useful life and disposed of normally, the RBC disintegrates in a manner allowing free iron-containing molecules to reach the blood. With their complete lack of mitochondria, RBCs rely on pentose phosphate pathway (PPP) for the materials needed to reduce oxidative damage. Any limitations of PPP can result in more susceptibility to oxidative damage and a short or abnormal lifecycle. If the cell is unable to signal to the reticuloendothelial phagocytes by externalizing phosphatidylserine, it is likely to lyse through uncontrolled means.The distinguishing feature of intravascular hemolysis is the release of RBC contents into the blood stream. The metabolism and elimination of these products, largely iron-containing compounds capable of doing damage through Fenton reactions,  is an important part of the condition. Several reference texts exist on the elimination pathways, for example. Free hemoglobin can bind to haptoglobin, and the complex is cleared from the circulation; thus, a decrease in haptoglobin can support a diagnosis of hemolytic anemia. Alternatively, hemoglobin may oxidize and release the heme group that is able to bind to either albumin or hemopexin. The heme is ultimately converted to bilirubin and removed in stool and urine. Hemoglobin may be cleared directly by the kidneys resulting in fast clearance of free hemoglobin but causing the continued loss of hemosiderin loaded renal tubular cells for many days. Additional effects of free hemoglobin seem to be due to specific reactions with NO.