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Hip dysplasia is an abnormality of the hip joint where the socket portion does not fully cover the ball portion, resulting in an increased risk for joint dislocation. [4] Hip dysplasia may occur at birth or develop in early life. [4] Regardless, it does not typically produce symptoms in babies less than a year old. [5]
Dysplasia can affect all three lineages seen in the bone marrow. The best way to diagnose dysplasia is by morphology and special stains used on the bone marrow aspirate and peripheral blood smear. Dysplasia in the myeloid series is defined by: Granulocytic series [citation needed]:
Thanatophoric dysplasia is a severe skeletal disorder characterized by a disproportionately small ribcage, extremely short limbs and folds of extra skin on the arms and legs. Symptoms and signs [ edit ]
Other symptoms may include hypoesthesia, paresthesia, and discomfort. [3] In rare instances, patients may experience associated facial swelling with the presence or absence of pain due to concurrent infection. [4] Patients experiencing symptoms also tend to be older and have the periapical form of cemento-osseous dysplasia. [3]
Acromesomelic dysplasia is a rare skeletal disorder that causes abnormal bone and cartilage development, leading to shortening of the forearms, lower legs, hands, feet, fingers, and toes. [2] Five different genetic mutations have been implicated in the disorder.
[1] [2] There are over 200 different syndromes classified under ED, each with a range of symptoms and genetic causes. [3] The most common type is Hypohidrotic Ectodermal Dysplasia (HED), which affects approximately 1 in every 5,000 to 10,000 live births. HED primarily affects males because it is typically inherited through the X chromosome. [2] [3]
The signs and symptoms of spondyloepiphyseal dysplasia congenita are similar to, but milder than, the related skeletal disorders achondrogenesis type 2 and hypochondrogenesis. Spondyloepiphyseal dysplasia congenita is a subtype of collagenopathy, types II and XI .
The cause of CIN is chronic infection of the cervix with HPV, especially infection with high-risk HPV types 16 or 18. It is thought that the high-risk HPV infections have the ability to inactivate tumor suppressor genes such as the p53 gene and the RB gene, thus allowing the infected cells to grow unchecked and accumulate successive mutations, eventually leading to cancer.