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  • The osteoid and woven bone

    2019-04-15

    The osteoid and woven bone can be seen as interconnected trabeculae (thin or broad) or sheets. The bone surrounding the lesion (host bone) is strong and is made of varying mixtures of woven and lamellar bone [36]. The radiologic appearance of cortical osteoid osteoma arising in the shaft of a long bone has certain characteristics. It may be radiolucent and contain a changeable amount of mineralisation and is usually centrally positioned in an area of reactive osteosclerosis (dense fusiform, reactive). Sclerosis may regress after surgical removal of the tumour. Preoperative administration of tetracycline and the use of UV light for examination during the procedure may enhance the surgeon׳s view of the nidus. This technique works due to the tetracycline׳s position in the rapidly metabolised osteoid of the nidus in contrast to the slow mineralising host bone [36]. Out of 860 cases reviewed by Jackson et al. only 1.6% found it painless [39]. Most patients present with a swelling, mass or deformity. Swelling may be associated with superficial lesions. Table shows the anatomical locations of the osteoid osteomas and their characteristics:
    Aneurysmal bone cyst Aneurysmal bone cysts (ABCs) are fairly rare benign cystic lesions, accounting for approximately 9.1% of all bone tumours [41]. The blood filled cysts are divided by myc pathway septa and contain a mix of osteoclasts, giant cells, and reactive woven bone [42–44]. Controversy exists as to the pathogenesis of aneurysmal bone cysts. In 30% of cases a predisposing lesion can be identified, a finding that some argue suggests that aneurysmal bone cysts are a reactive process to other pathological changes, rather than a distinct tumour type [42,44]. The most common pre-existing lesion is the giant cell tumour [44]. The sites most commonly associated with ABC are the femur, tibia, humerus and fibula, although they can present in other sites [42]. ABC appears on radiographs as radiolucent lesions of eccentric origin in the metaphysis of long bones [42]. The term ‘soap bubble’ is used to describe these lesions, a description which describes the erosion of the cortex of the bone and elevation of the periosteum [43]. CT imaging can be helpful in identifying the margins of the cyst [21]. MRI allows identification of the thin septa dividing the cyst, as well as demonstrating fluid-fluid levels within the cyst [42]. Biopsy and histological examination of the ABC is necessary to confirm the diagnosis [41,42]. There are a number of management options for ABCs. Curettage with bone grafting or resection and reconstruction for eccentric lesions has traditionally been used [43]. Curettage often involves adjuvant therapy to reduce the recurrence rate, which may be as high as 31% [41]. This may involve sclerotherapy [45] or cryotherapy, which has been shown to reduce the recurrence rate to 5% [46]. Embolization procedures, namely the injection of alcohol zein or selective arterial embolization, are highly controversial [41]. A number of novel potential treatments for ABC have recently been described in case studies. These treatments are less invasive and thus may offer an advantage over aggressive surgical options. The use of Denosumab as a therapeutic agent for the treatment of ABCs has been described in a study involving two patients with ABCs at C5, who both displayed tumour regression at 2 or 4 months [47]. However, more research in this area is required. New graft material such as autologous bone marrow mononuclear cells combined with B -tricalcium phosphate and atelocollagen has also resulted in ossification of the cyst in one patient [48]. These case studies show potential for resulting in innovative treatments for ABC, however more extensive trials are necessary before firm conclusions can be drawn.
    Fibrous dysplasia Fibrous dysplasia (FD) accounts for 5–7% of all benign bone tumours [49]. Fibrous dysplasia presents in two main forms – monostotic, affecting one bone, or polyostotic, which affects several bones. 75% of cases of fibrous dysplasia are of the monostotic form [50]. Monostotic fibrous dysplasia typically affects those in their 3rd decade of life, whist polyostotic presents in the 1st decade [51]. Polyostotic FD commonly affects the craniofacial bones, but may also affect the ribs, femur or tibia [51]. Fibrous dysplasia consists of fibrous stroma with a cellular component, with mutated fibroblast cells and osteoblasts of varying functionality, which produce abnormally shaped trabeculae of woven bone [51,52]. FD mostly becomes dormant as the affected child moves into adulthood, however there is a lifetime risk of malignant transformation that of around 1–4% [53].