1. INTRODUCTIONThe paranasal sinuses include the ethmoid, frontal, sphenoid, and maxillary sinuses. These air-filled spaces in the maxillofacial and skull area are lined with mucosa and communicate with the nasal cavity (1). The maxillary sinuses start developing in the third month of intrauterine life, making them the first paranasal sinuses to develop in the human fetus (2). They continue to grow until puberty. The maxillary sinus typically has an average volume of 6-8 cm³, making it the largest paranasal sinus, though its size varies with age (3).Maxillary sinus aplasia (MSA) is a condition characterized by the absence of sinus development. This rare condition is often asymptomatic but can sometimes present as facial pain or headaches. Typically diagnosed incidentally during radiological procedures for other purposes, such as dental implants, MSA shows no gender or geographical predilection and can occur worldwide (4). MSA may occur in isolation or be associated with broader craniofacial syndromes like cleft palate, Crouzon syndrome, or Apert syndrome. While many individuals with MSA are asymptomatic, those with symptoms may experience nasal obstruction, sinus infections, or facial pain (5). Symptomatic management focuses on addressing related nasal or sinus issues, and surgical intervention is rarely needed, reserved only for specific complications or associated craniofacial abnormalities (6). Hypoplasia of the inferior concha and the absence of the infundibulum and uncinate process are rare anatomical variations that can significantly impact clinical outcomes, particularly in cases of MSA or other sinus anomalies (7). Often discovered incidentally during imaging, these conditions can be asymptomatic but may sometimes present with sinonasal symptoms like nasal obstruction or chronic sinusitis. Case reports highlight the association of these anomalies with impaired sinus function and recurrent infections, necessitating careful evaluation and tailored management strategies (8).Maxillary sinus hypoplasia (MSH) refers to the underdevelopment of the maxillary sinuses, where the sinus is present but smaller than normal. This condition can affect individuals of any age and gender and is often discovered incidentally (9). Symptomatic individuals may experience chronic or recurrent sinus infections, nasal obstruction, or facial pain, particularly in the cheek area. MSH can also be associated with other craniofacial anomalies or developmental conditions like cleft palate and craniosynostosis syndromes (10). MSH is classified into three types according to Bolger’s classification: Type I (mild hypoplasia), Type II (significant hypoplasia with an absent uncinate process), and Type III (profound hypoplasia with an absent uncinate process). CT scans are the gold standard for diagnosing MSH and MSA, with MRI also being useful (11). Symptomatic cases are treated with medical management, including antibiotics, nasal decongestants, and corticosteroids (9). For chronic or recurrent sinusitis unresponsive to medical treatment, functional endoscopic sinus surgery (FESS) may be considered to improve sinus drainage and ventilation. Asymptomatic cases do not require treatment. An incidental finding of unilateral maxillary sinus aplasia was reported during a radiographic examination (8, 9). We report an incidental finding of unilateral aplasia of the maxillary sinus during a radiographic examination.

1. INTRODUCTIONA giant cell tumor (GCT) is a benign neoplasm characterized by progressive and destructive features. Typically manifesting in individuals during their third or fourth decade of life, GCT exhibits a higher prevalence in women than in men. Although categorized as a benign bone tumor, GCT displays local aggressiveness and a propensity for recurrence (1). Accounting for approximately 6% of all bone tumors, 4% of primary bone tumors, and 20% of benign bone tumors, GCTs are relatively uncommon. The distal femur, proximal tibia, and distal radius are the most frequently affected long bones, with a particular predilection for the distal end of the radius, making it the third most common location for GCT after the distal femur and proximal tibia. Despite their benign classification, GCT can exhibit local aggressiveness, causing bone erosion, pain, and potentially leading to fractures (2).GCT or osteoclastoma, is a rare yet locally aggressive primary bone tumor characterized by multinucleated giant cells dispersed throughout the tumor, along with mononuclear stromal cells producing osteoid matrix. Histologically, GCT exhibits areas of hemorrhage and necrosis indicative of its aggressive nature, and in some cases, increased mitotic activity (3). The stromal cells often generate fibrous bands and septae, contributing to tumor compartmentalization. Histological grading based on features like mitotic activity guides prognosis, with higher grades associated with increased recurrence rates. Immunohistochemistry, utilizing markers such as CD68, CD163, and RANKL, aids in distinguishing GCT from other bone tumors. Understanding these histopathological features is crucial for accurate diagnosis and management decisions, which often involve a multidisciplinary approach tailored to the tumor’s behavior and grade (4).GCTs pose a challenge in terms of management, especially when located in the distal radius. En bloc resection, a surgical technique involving the removal of the tumor along with a margin of surrounding normal tissue, is often employed in cases of large, aggressive, or challenging-to-reach tumors. This method aims to reduce the risk of local recurrence (5). However, the optimal approach for treating GCTs of the distal radius remains controversial, with en-bloc excision showing decreased recurrence but posing challenges for wrist reconstruction due to the complex functional requirements of the wrist (6). The multidisciplinary management of GCTs involves various treatment options such as curettage, cryotherapy, radiation therapy, monoclonal antibody therapy (Denosumab), and surgery. Recurrence rates after surgical treatment may vary based on factors like tumor location, extent of surgical resection, and patient age. Distal ulna and radius have been reported as especially susceptible to GCT recurrence after resection (7).This study aims to provide a comprehensive overview of different reconstruction techniques employed after en-bloc resection of GCTs in the distal radius, acknowledging the controversies and varied opinions among orthopedic oncologists on the most effective strategies for managing long bone defects.

A document by Habib Azimi. Click on the document to view its contents.

1. INTRODUCTIONOsteochondromas (OC) are benign tumors that account for 20-50% of benign and 10% of all bone tumors. The incidence rate of OC in males is twice that of females and its peak is usually in the second decade of life (1). These lesions are inherited in an autosomal dominant manner and cause the formation of isolated lesions or multiple exostoses during the development of bones in the process of enchondral ossification in the long bones (2). Also, OC is associated with the mutation of some tumor suppressor genes, including EXT1 or EXT2 genes. OC have a periosteal origin and are formed in the active parts of bones, including the metaphysis of long bones and the cartilage at their ends. Studies show that OC can be caused after surgery/radiation-induced injury and hematopoietic stem cell transplantation (3).Osteocartilaginous exostosis is mainly detected in childhood and in the form of palpable masses, with chronic pain and sometimes with edema (4). The presence of misplaced bone masses in the joint capsule and sometimes with cartilaginous coating in radiographic images is one of its common manifestations. The most common joints involved in OC are the hip and knee joints. Patellar OC is rare and mostly affects the patellar bursa. Moraes et al. (2014) reported a patellar OC measuring 8 × 6 × 3 cm anterior to the patella in a 60-year-old man who was painless and without limitation of flexion-extension in the knee joint (5). In the present case, rare retro-patellar OC was observed in the area of the patellar ligament.

1. INTRODUCTIONIntramuscular myxoma (IMM) are benign soft tissue that account for 0.1 to 0.13 per 100,000 populations (1). Various theories have been described regarding the mechanism of IMM occurrence. Some researchers suggest that the reason is fibroblasts (unable to synthesize collagen fibers) that are not well differentiated from mesenchymal stem cells, which cause the synthesis of myxoid stroma without reticular fibers. Others consider the etiology of IMM to be caused by traumatic mechanisms or the growth of polysaccharide-producing cells in the neoplastic process (2). IMM is rare and can occur in the buttocks, thigh, upper extremities and shoulder muscles. Epidemiologically, its occurrence rate is higher in women (70%), increases with age (6th and 7th decade of life) and the most common sites of IMM is upper extremities muscles (50%-60%) (3). According to the location of the masses, soft-tissue myxomas are classified into superficial angiomyxoma, intramuscular myxoma, nerve sheath myxoma and aggressive angiomyxoma. From the clinical point of view, IMM is a palpable mass, painless, without inflammatory secretions and symptoms, which has no contractile properties and no stretch-contraction changes during flexion-extension of the adjacent muscles (4).From a diagnostic point of view, IMM is observed as a non-calcified mass in plain radiograph, which is seen in the supplementary findings with the help of ultrasonography as echogenic cystic lesions among the muscle tissue. The most important diagnostic method of IMM from other soft tissue lesions is magnetic resonance imaging (MRI), which can be seen as hypointense homogeneous mass in T1-weighted sections and hyperintense in T2-weighted sections (5). In case of edema with IMM in MRI sections (T1-weighted sections), it should be differentiated from other fluid-containing lesions (such as cystic teratoma, hematoma, myxoid sarcoma, cystic hygroma and even normal lymph nodes). Also, IMM should be differentiated from proliferative lesions, other myxoid neoplasms, myxochondroma, myxochondroma and myxoid liposarcoma (6). Cytology-histopathology findings with the help of intraoperative frozen section and needle biopsy help the information of MRI sections in the diagnosis of IMM. Density and ratio of cells/ collagen fibers, mucoid material secretion, nodular-vesicular pattern and fat density in histopathological sections contribute to IMM (7). In the present case, forearm intramuscular myxoma was observed inter-supinator muscle.