The collagen fibril and EDS: (a) Normal collagen fibrils are of uniform size and spacing. Fibrils from a person with dermatosparaxis (b) show dramatic alterations in fibril morphology with severe effects on the tensile strength of connective tissues. A person with classical EDS (c) shows composite fibrils. Fibrils from a TNX-deficient person (d) are uniform in size and no composite fibrils are seen. TNX-null (e) fibrils are less densely packed and not as well aligned to neighboring fibrils. Every type of EDS, except the hypermobile type (which affects the vast majority of people with EDS), can be positively tied to specific genetic variation. Variations in these genes can cause EDS: * Collagen primary structure and collagen processing: ADAMTS2, COL1A1, COL1A2, COL3A1, COL5A1, COL5A2 * Collagen folding and collagen cross-linking: PLOD1, FKBP14 * Structure and function of myomatrix: TNXB, COL12A1 * Glycosaminoglycan biosynthesis: B4GALT7, B3GALT6, CHST14, DSE * Complement pathway: C1R, C1S * Intracellular processes: SLC39A13, ZNF469, PRDM5 Variations in these genes usually alter the structure, production, or processing of collagen or proteins that interact with collagen. Collagen provides structure and strength to connective tissue. A defect in collagen can weaken connective tissue in the skin, bones, blood vessels, and organs, resulting in the features of the disorder. Inheritance patterns depend on the specific<unk>  Most forms of EDS are inherited in an autosomal dominant pattern, which means only one of the two copies of the gene in question must be altered to cause a disorder. A few are inherited in an autosomal recessive pattern, which means both copies of the gene must be altered for a person to be affected by a disorder. It can also be an individual (de novo or "sporadic") variation. Sporadic variations occur without any inheritance.
Ehlers–Danlos syndromes
Hypermobility (joints)
Ogden syndrome
Cutis laxa
Marfan syndrome
Hypermobility spectrum disorder
Dennie–Marfan syndrome
Lelis syndrome