A 64 year-old-man was referred to the hospital because of dry cough since 2 weeks. The patient was an ex-smoker, smoking 2 packs per day for 40 years. His medical history revealed hypertension treated with anti-hypertensive agents. The patient was conscious and alert, with body temperature 36.5  C, heart rate 122 bpm, and blood pressure 147/88 mmHg. Oxygen saturation was 93% in room air. Coarse crackles were detected bilaterally on chest auscultation. He had felt multiple arthralgias on the limbs symmetrically without swelling or deformation. Chest X-ray showed infiltration of the both lung fields (Fig. 1a). Chest computed tomography revealed the non-segmental patchy shadow and consolidation on both sides (Fig. 1b). The white blood cell count was 17,500 cells/muL and C-reactive protein level was 26.5 mg/dL. The patient was diagnosed with community-acquired pneumonia, and was subsequently treated with ampicillin/sulbactam and pazufloxacin. Blood and sputum cultures were negative, whereas anti-cyclic citrullinated peptide antibody (anti-CCP Ab) was elevated significantly. Antibiotic treatment was ineffective. Bronchoscopy, performed for more thorough examination, revealed white and soft tissues scattered in the trachea that could not be removed by suction or forceps (Fig. 2a). Purulent sputum was absent. Pathological and bacteriological evaluation of the tracheal lesions and lung was performed. Specimens of tracheal mucosa revealed findings consistent with NTB indicated by necrotic tissue with squamous metaplasia and inflammatory cells of tracheal tissue (Fig. 2b). However, the findings did not confirm chondritis. No specific pathogen was identified with PAS or Grocott and Ziehl-Neelsen staining. Lung biopsy indicated organizing pneumonia (OP), whereas eosinophilic leukocytosis and vasculitis were not observed. The patient was diagnosed with NTB and OP. Moreover, diagnosis of RA was determined results of rheumatoid factor and anti-CCP Ab tests, and evaluation of joints' manifestations by orthopedist. After the bronchoscopy, an acute exacerbation of the respiratory condition developed. Immediately, steroid pulse therapy and oxygen therapy were started. Then the both clinical condition were gotten stability. Repeat bronchoscopy to observe the tracheal lesion indicated resolution of scattered lesions without scarring; while, re-biopsy samples of trachea showed persistent necrosis. Subsequent, chest radiography indicated improvement (Fig. 3a and b).