Adult Scheuermann’s disease as cause of mechanic dorsalgia

Trotta, A.; Corrado, Antonio; Soragnese, M.F.; Santoro, Nanette; Cantatore, Francesco Paolo

doi:10.4081/reumatismo.2008.14

Cited by 4 publications

(3 citation statements)

References 39 publications

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“…In fact, the most accepted male to female ratio is between 2:1 and 7:1 ( 23 ). The age onset of SK is between 10 and 12 years old but an adulthood onset is not unheard of ( 24 ). Although the kyphosis angle was not influenced by sex, it was positively correlated to the age ( 25 ).…”

Section: Natural Historymentioning

confidence: 99%

Scheuermann's kyphosis: update on pathophysiology and surgical treatment

et al. 2022

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Scheuermann’s Kyphosis (SK) is a rigid spinal kyphosis. Several theories have been proposed concerning its pathogenesis, but it is, to this day, still unknown. It has a prevalence of 0.4–8.3% in the population with a higher incidence in females. Clinical examination with x-rays is needed to differentiate and confirm this diagnosis. Non-surgical management is reserved for smaller deformities and in skeletally immature patients, whereas surgery is recommended for higher deformities. Combined anterior and posterior approach was considered the gold standard for the surgical treatment of this disease, but there is an increasing trend toward posterior-only approaches especially with use of segmental fixation. This study reviews the pathophysiology of SK while proposing a treatment algorithm for its management.

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Section: Natural Historymentioning

confidence: 99%

Scheuermann's kyphosis: update on pathophysiology and surgical treatment

et al. 2022

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“…In some cases, especially when the pathology is present at the lumbar level, spine osteochondrosis is asymptomatic, and the related LBP can appear only in adulthood [ 6 , 7 , 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

“…The etiology of osteochondrosis is elusive, and likely multifactorial. Evidence highlights the involvement of an impaired blood supply causing oxygen and nutrition insufficiency at the vertebral ossification nuclei and consequent cell necrosis [ 4 ], but mechanical damage/repeated microtrauma can also contribute [ 8 ]. Moreover, a genetic influence was observed: a high prevalence of osteochondrosis in male monozygotic twins [ 16 , 17 ] and an inheritance of the autosomal dominant type [ 18 , 19 ] support the genetic etiology hypothesis.…”

Section: Introductionmentioning

confidence: 99%

High Levels of Circulating Type II Collagen Degradation Marker (CTx-II) Are Associated with Specific VDR Polymorphisms in Patients with Adult Vertebral Osteochondrosis

Cauci

Viganò

Luca

et al. 2017

IJMS

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Both vitamin D and collagen have roles in osteocartilaginous homeostasis. We evaluated the association between the circulating 25-hydroxyvitamin D (25(OH)D), type I and II collagen degradation products (CTx-I, and CTx-II), and four vitamin D receptor gene (VDR) polymorphisms, in Italian males affected by low back pain (LBP) due to herniation/discopathy and/or vertebral osteochondrosis. FokI, BsmI, ApaI, and TaqI VDR-polymorphisms were detected through PCR–restriction fragment length polymorphism (RFLP), and circulating 25(OH)D, CTx-I and CTx-II were measured by immunoassays in 79 patients (of which 26 had osteochondrosis) and 79 age-, sex- and body mass index (BMI)-matched healthy controls. Among all 158 subjects, carriers of FF and Ff genotypes showed lower 25(OH)D than ff, which suggested a higher depletion of vitamin D in F allele carriers. Higher CTx-I concentrations were observed in TT versus Tt among controls, and Tt versus tt among LBP cases, which suggested a higher bone-cartilaginous catabolism in subjects bearing the T allele. Higher CTx-II concentrations were observed in patients with osteochondrosis bearing FF, bb, TT, or Aa genotypes in comparison with hernia/discopathy patients and healthy controls. Vertebral osteochondrosis shows peculiar genotypic and biochemical features related to vitamin D and the osteocartilaginous metabolism. Vitamin D has roles in the pathophysiology of osteochondrosis.

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