Cemento-ossifying fibroma (COF) is classified as a fibro-osseous lesion and usually presents as a progressively growing lesion that can reach a large size if left untreated. Fibrous dysplasia (FD) is a non-neoplastic development that affects the craniofacial bones and is characterized by painless hypertrophy due to the replacement of bone by abnormal fibrous tissue. Herein, a case of concurrent occurrence of COF and FD involving the right mandible is described in a 14-year-old male patient. In this review, the current knowledge of FD and COF is summarized, emphasizing the importance of integrating the understanding of clinical, radiographic, and histopathological features. In addition, the relevant aspects associated with differential diagnosis and patient care are evaluated.

Sarcomatous transformation of fibrous dysplasia (FD) is rare and can occur in patients with McCune-Albright syndrome (MAS). To date, there have been several cases of malignant transformation of FD in the craniofacial area of patients with MAS. Here, we report an additional case of secondary osteosarcoma arising from FD in the mandible of a 41-year-old woman with MAS. The patient complained of rapid swelling in the right facial area, which was initially misdiagnosed as soft tissue sarcoma at another hospital. After neoadjuvant concurrent chemoradiotherapy resulting in poor response, the lesion was surgically resected in our hospital, and the final diagnosis of secondary osteosarcoma was rendered. Currently, post-operative adjuvant chemotherapy is in progress. As a result of our review of 17 reported cases showing malignant transformation in FD/MAS, the M/F ratio was 1:1.1, and the median age at onset of malignancy was 28.6 years. The most commonly affected site was the craniofacial bones (n=13; 76%), and the most common histopathologic type of malignancy was osteosarcoma (n=14; 82%). More than half of the patients (8/15; 53.3%) died within 1 year, mainly due to lung metastasis (6/8; 75%). Taken together, since MAS patients with malignant transformation of FD have a relatively poor prognosis, accurate diagnosis based on histopathologic findings as well as clinical and radiographic information is important to select optimal treatment.

Benign fibro-osseous lesions are demonstrated as a group of conditions, which normal bone is replaced by a connective tissue matrix that gradually develops cemento-osseous tissue and include developmental lesion, reactive lesion, dysplasia and tumor. Cemento-osseous dysplasia is one of benign fibro-osseous lesions, which is non-neoplastic process. Histologic features of cemento-osseous dysplasia are admixtures of bone and cementoid materials in a fibrous stroma. Cemento-osseous dysplasia associated with traumatic bone cysts has infrequently been reported. Traumatic bone cyst is a pseudocyst that may befound in both the jaws and the long bones. Though blockage of interstitial fluid drainage orvenous obstruction may be the cause of traumatic bone cyst, the exact pathogenesis of traumatic bone cysts is unknown. Melrose et al. was the first to report association of cemento-osseous dysplasia and traumatic bone cystsin their series. It is assumed that different mechanism is involved in cyst formation in these cases. This report presents review of literature and describes a case of focal cemento-osseous dysplasia associated with traumatic bone cyst of the mandible and its surgical treatment.

Florid cemento-osseous dysplasia (FCOD) is benign and exhibits multifocal involvement of tooth-bearing areas of the jaw. Initially, the lesions are radiolucent but become mixed. In late stages, the lesions change into a radiopaque mass with a thin radiolucent rim. Most FCOD cases are asymptomatic, and conservative treatment is recommended. However, surgical intervention is necessary in secondary infected cases. Because of hypovascularity, infected lesions are difficult to manage and do not respond to antibiotic medications. This clinical report describes the treatment of secondary infection of an FCOD lesion with both conservative and surgical interventions.

Renal dysplasia is a developmental disorder of the renal parenchyma involving anomalous differentiation. It is characterized by persistent metanephric ducts surrounded by primitive mesenchyme, fetal or immature glomeruli, fetal or immature tubules, interstitial fibrosis, and dysontogenic metaplasia involving tissues such as cartilage. Renal dysplasia has been rarely reported in rats. Here, we observed a small left kidney in a rat used in a short-term repeat toxicity study. The rat showed no clinical signs throughout the study. All parameters, including those reflecting kidney functions, were normal upon hematological examination and urinalysis. Grossly, the kidney was small (5 × 8 mm) and its surface appeared normal. Histological examination revealed that the cortex and medulla were poorly demarcated and contained immature/atrophic glomeruli, immature renal tubules, and mesenchymal cells. The cortex contained immature glomeruli, atrophic glomeruli with cystic dilatation of Bowman’s capsular space, and some atypical tubules. Primitive metanephric tubules in the medulla were larger in diameter than normal collecting ducts, lined by a tall columnar epithelium with pale cytoplasm and basal nucleus, and surrounded by loose mesenchymal cells. Occasional tubules contained pale eosinophilic homogenous material in the lumen. Thus, this was diagnosed as a case of renal dysplasia on the basis of histologic features and is the first reported case of renal dysplasia in Sprague Dawley rats.

Oral squamous cell carcinoma (OSCC) develops through multistep process, that is, from normal mucosa to hyperplastic area and progressed to dysplasia, carcinoma in situ, and finally to invasive carcinoma. The purpose of this study is to investigate the histological types of the transitional area from normal oral mucosa to invasive carcinoma for the baseline data to search intermediate end point markers for early detection of OSCC. For this purpose, we reviewed the 85 patients who were diagnosed as OSCC in the Department of Oral Pathology, Yonsei University College of Dentistry, from 2002 to 2008. We classified these histopathologic findings by light-microscopy, according to the histologic pattern of transitional areas. As results, stepwise transformation from normal oral mucosa, to dysplasia and to OSCC was shown in 47 patients. Intermittent lesions were seen in 16 patients, in which normal oral mucosa, dysplasia, and OSCC were alternately arranged. Twenty two patients showed abruptly transformed to OSCC from normal oral mucosa. These preliminary data will be used for searching biomarkers for early detection of OSCC.

Osteogenic sarcoma is primary malignant bone tumor. It can arise de novo or from the benign precursors lesions, like Paget’s disease, giant cell tumor, chronic osteomyelitis, osteoblastoma, and fibrous dysplasia. Here, we present a case of osteogenic sarcoma arising from florid osseous dysplasia appearing as a rapidly growing bony bulging mass in 44‐year‐old Korean female who had at first been non‐symptomatic, but later suffered from the numbness of chin and lower lip. The radiologic images revealed the mixed radiopaque‐ radiolucent intraosseous lesions throughout the mandible, which were diagnosed as florid osseous dysplasia pathologically. But only after 6 months, the lesions were substituted by the radiological ill‐defined diffuse bony sclerotic lesion with bone destruction, accompanying the interrupted periosteal bone formation, which were pathologically diagnosed as osteogenic sarcomas. These serial clinicopathologic changes imply the malignant progression of florid osseous dysplasia rather than the collision of benign condition, florid osseous dysplasia and malignant tumor, osteogenic sarcoma. The possibility for fibro‐osseous lesion of the jaw as premalignant lesion should not be overlooked; therefore, periodic check‐ups for the lesions are necessary. Proper evaluation and interpretation for clinical neural symptom and radiologic change of bone density may lead to the correct differential diagnosis and therapeutic intervention.

Dysplasia-associated seizure disorders are markedly resistant to pharmacological intervention. Relatively little research has been conducted studying the effects of antiepileptic drugs(AEDs)on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate(MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of AEDs in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed and age-matched vehicle-injected control animals. Field potential recordings were used to monitor amplitude and numbers of population spikes, and paired pulse inhibition in response to stimulation of commissural pathway. Two commonly used AEDs were tested: diazepam 5, 2.5 mg/kg; phenytoin 40, 60 mg/kg. Diazepam(DZP) and phenytoin(PHT) reduced the amplitude of population spike in control and MAM-exposed rats. However, the amplitude of population spike was nearly eliminated in control rats as compared to the MAM-exposed rats. Pharmaco-resistance was tested by measuring seizure latencies in awake rats after pilocarpine administration(320 mg/kg, i.p.) with and without pretreatment with AEDs. Pre-treatment with PHT 60 mg prolonged seizure latency in control rats, but not in MAM-exposed animals. The main findings of this study are that acute seizures initiated in MAM-exposed rats are relatively resistant to standard AEDs assessed in vivo. These data suggest that animal model with cortical dysplasia can be used to screen the effects of potential AEDs.

Florid cemento-osseous dyspl잃ia with concommitant traumatic bone cyst is uncommon condition. We report a case of florid cemento 。，sseous dysplasia involving four quadrants of the jaws and associated with large cystic lesion of the mandible misdiagnosed as a multiple odontogenic keratocysts in a 37-year-old Korean woman. Histological examination revealed unencapsulated fibroblastic proliferation with formation of bone and cementum, showing different developmental stages, and cys디c lesions resembling a traumatic bone cyst.

Developmental dysplasia or dislocation of the hip is the most pronounced form of a condition in which the femoral heads tends progressively to leave the acetabulum. In the young child the variability of findings and course suggest a spectrum of conditions in which there are a number of common features: restriction of movement, particularly of abduction in flexion; shortening; and abnormal radiology, including a sloping or dysplastic acetabulum and delay in the appearance of the upper femoral epiphysis. It is vital to make the diagnosis of a congenital dislocation as soon after birth as possible. Conservative treatment with an abduction brace before the child run begins to walk is completely adequate, but after the age of 4 even surgical repositioning is difficult and after the age of 7 it is almost impossible. The aim of the study was to gain insight into the value of physical therapy of developmental dysplasia or dislocation after operation.