Disease relevance of Hyperostosis

• Sclerosteosis is an uncommon, autosomal recessive, progressive, sclerosing, bone dysplasia characterized by generalized osteosclerosis and hyperostosis of the skeleton, affecting mainly the skull and mandible [1].
• Therefore, our patient's extensive oropharyngeal exostoses and endosteal hyperostosis likely reflect increased Wnt signaling and show that exuberant LRP5 effects are not always benign [2].
• The diagnostic value of hyperostosis in midline subfrontal meningioma [3].
• Palaeopathology of spinal osteophytosis, vertebral ankylosis, ankylosing spondylitis, and vertebral hyperostosis [4].
• Cortical hyperostosis following long-term administration of prostaglandin E1 in infants with cyanotic congenital heart disease [5].

High impact information on Hyperostosis

• These data suggest that: (a) the hyperostosis and the metaphyseal long bone deformity in the present CMD patient might be explained by osteoclast dysfunction due to impaired expression of the osteoclast-reactive vacuolar proton pump; and (b) a protooncogene c-src was not associated with the pathogenesis of the present CMD patient [6].
• Spinal hyperostosis and etretinate [7].
• This region was analyzed because of the recent assignment to this chromosomal region of the gene causing van Buchem disease, a rare autosomal recessive condition with a hyperostosis similar to sclerosteosis [1].
• Calcium pyrophosphate dihydrate crystal deposition disease with concurrent vertebral hyperostosis in a Barbary ape [8].
• A naturally occurring nonsense truncation mutation of the inorganic pyrophosphate (PPi)-generating nucleoside triphosphate pyrophosphohydrolase (NTPPPH) PC-1 is associated with spinal and periarticular ligament hyperostosis and cartilage calcification in "tiptoe walking" (ttw) mice [9].

Chemical compound and disease context of Hyperostosis

• Diffuse hyperostosis associated with etretinate [10].
• A total of 63 patients (95%) showed varying degrees of hyperostosis involving the cribiform plate, planum sphenoidale, or tuberculum sellae (including the chiasmatic sulcus) [3].
• Appearance of hyperostosis frontalis interna on indium-111 leukocyte scans: potential diagnostic pitfall [11].
• Cortical hyperostosis after administration of prostaglandin E [12].
• As a result, complications of prolonged PGE1 infusion, such as cortical hyperostosis, are being encountered more commonly [13].

Biological context of Hyperostosis

• Ossification of the posterior longitudinal ligament, diffuse, idiopathic skeletal hyperostosis, abnormal retinol and retinol binding protein: a familial observation [14].
• Tibial bone histomorphometry revealed high-turnover osteopenia in group C, significant improvement in both bone formation and resorption parameters in group D and hyperostosis in group B. Serum BGP reflected the histomorphometric indices of bone formation in each group.(ABSTRACT TRUNCATED AT 250 WORDS)[15]

Anatomical context of Hyperostosis

• There have been a very few reports where a tendency of hyperostosis was observed for ossification of the spinal ligaments such as OPLL, OYL and ASH [16].

Gene context of Hyperostosis

• The twy mouse displays elevated osseous formation particularly in the spine, and the pathophysiological features resemble that of human ankylosing spinal hyperostosis [17].
• It was found that the retinol level of plasma decreased in patients of both sexes suffering from rheumatoid arthritis and clinically active ankylosing spondylitis, but increased in female patients suffering from ankylosing hyperostosis connected with diabetes, and also in the diabetes group [18].
• A generalized skeletal hyperostosis in two siblings caused by a novel mutation in the SOST gene [19].
• Craniometaphyseal dysplasia--Jackson type (CMDJ) is an autosomal dominant bone dysplasia with hyperostosis and sclerosis of the skull and abnormal modelling of the metaphyses [20].
• Significantly increased BMD was observed in patients with ankylosing spinal hyperostosis (ASH) in addition to OPLL [21].

Analytical, diagnostic and therapeutic context of Hyperostosis

• Prostaglandin-induced subperiosteal hyperostosis should now be considered in the differential diagnosis of neonatal cortical proliferation [22].
• The method has been successfully applied to the analysis of both isomers in serum from patients with idiopathic skeletal hyperostosis in whom, the 13-cis- as well as all-trans-retinoic acid levels were raised as compared to the control group [23].
• Abnormal whole-body technetium-99m MDP scintigraphy indicating cortical hyperostosis following long-term administration of prostataglandin E-1 in an infant with cyanotic congenital heart disease [24].

References