Navajo familial neurogenic arthropathy (NFNA) is a rare form of hereditary sensory autonomic neuropathy found in the Navajo population. It usually becomes clinically apparent during the first two decades of life, with unrecognized fractures, Charcot joints as a result of sensory deficits to deep pain, hypohidrosis, and heat intolerance1. Orthopaedic manifestations secondary to NFNA have been described2; however, to the best of our knowledge, reports of treatment outcomes in the literature are limited. An online database search on MEDLINE was conducted with the words “Navajo Familial Neurogenic Arthropathy” as Medical Subject Headings and keywords. Because of the limited amount of published information on the subject matter, no language restrictions or limitations were applied. This case report describes a fifteen-year-old Native American boy with NFNA that resulted in complete destruction of the right knee. He was treated with knee arthrodesis; follow-up occurred nearly two years postsurgery. Despite residual limb-length inequality and peroneal nerve palsy, knee arthrodesis restored the boy’s ability to walk. The patient and his parents were informed that data concerning the case would be submitted for publication, and they provided consent. An eight-year-old Navajo boy presented for pediatric orthopaedic consultation with a painless right knee effusion several weeks after injuring the knee while wrestling with his father. The patient had no notable medical history, and there was no family history of musculoskeletal problems. It was noted that he frequently became overheated. Physical examination revealed a knee effusion, a posterior drawer sign, a positive Lachman sign of approximately 8 mm, and a grade-I pivot shift. The patient exhibited dry, thickened palmar and plantar skin, absent muscle stretch reflexes, and generalized lack of pinprick sensation. Radiographs of the knee revealed a large joint effusion, osseous sclerosis, and osseous defects involving the lateral femoral condyle and patella (Fig. …