Idiopathic avascular necrosis of the scaphoid bone, Preiser\'s disease, was originally described as a deteriorative pathology whereby the osseous structure necroses due to loss of blood supply. It may present with multifactorial etiology, which is still largely not well understood. We describe a case of Preiser\'s disease in a 70-year-old female, with worsening pain and loss of range of motion in her right wrist over a two-year period. Past medical history was significant for Sjogren\'s disease, fibromyalgia, and dystonia. Pain began several months following traumatic right dorsal wrist injury. Diagnosis of traumatic scaphoid fracture was originally suspected. Conservative treatment was unsuccessful. Radiographs did not demonstrate evidence of primary fracture. CT scan and MRI demonstrated osteonecrosis of the proximal pole of the scaphoid, but no evidence of fracture, either residual or healing, was found. Proximal row carpectomy was performed for avascular necrosis of the scaphoid. Histology confirmed diagnosis and verified absence of fracture. Postoperatively, the patient\'s pain and range of motion improved. This report combines histological findings of Preiser\'s disease with radiographic images which may ameliorate understanding of the clinical pathophysiology. We describe an unusual manifestation of Preiser\'s disease whereby a single traumatic event, in the absence of fracture, led to idiopathic scaphoid avascular necrosis, which may have been associated with Sjogren\'s syndrome and fibromyalgia. These conditions may have negatively impacted microvasculature and decreased bone mineral density, inversely correlated with the production of fatty marrow, facilitating the onset of osteonecrosis in the scaphoid.

Preiser\'s disease, also known as avascular necrosis of the scaphoid, is a rare condition that is incompletely understood in regard to pathophysiology, diagnosis, and management. There have been numerous case reports and case series evaluating a variety of conservative and operative interventions, but optimal treatment has not been well established. We describe the case of a 20-year-old female with stage II Preiser\'s disease that was managed with a vascularized bone graft from the 1,2 intercompartmental supraretinacular artery, in addition to temporary dorsal wrist-spanning bridge plate fixation. At the nine-year follow-up, the patient had near full wrist range of motion, no pain, and radiographs showing preserved carpal alignment and a scapholunate angle within normal range. Our findings suggest that this surgical technique is a viable option for restoring scaphoid vascularity, preserving carpal alignment, and halting disease progression.

The term Preiser\'s disease typically is used to describe idiopathic avascular necrosis of the scaphoid, but there have been a number of putative etiologies considered. It is rare and the natural history is not fully understood. Management of the condition should be based on patient factors as well as the stage of disease with regard to the scaphoid and the surrounding wrist. This chapter appraises the available evidence and aims to provide the reader with a framework to manage this rare condition.

Preiser\'s disease or aseptic necrosis of the scaphoid is a rare condition whose treatment, whether surgical or non-surgical, is not yet well defined. Its etiology remains unknown, and the treatment options depend on the disease\'s progression. Two classifications summarize the progress of this condition; the first by Hebert has four stages based on radiographic findings and the other by Kalainov defines two types according to extent of necrosis on MRI. A review of literature and our experience has led us to propose a decision-making algorithm for its therapeutic management, from conservative treatment to surgical treatment. The surgical procedure is chosen based on the disease stage and the extent of necrosis. According to Zaidemberg, in the early stages of the disease, treatment with a vascularized graft is the preferred solution. For more advanced stages, several techniques are available ranging from scaphoidectomy with potential prosthetic replacement or proximal row carpectomy to more radical solutions such as carpal arthrodesis. However, given the rarity of this disease, the indications for surgery remain tricky.

UNASSIGNED: An irreparable scaphoid proximal pole is challenging to treat because of the fragment size and limited blood supply. Salvage surgery, such as partial wrist fusion or proximal row carpectomy, may be performed but is not ideal for young patients. There are few reports of proximal scaphoid reconstruction using rib osteochondral grafts.
UNASSIGNED: Four patients were treated with rib osteochondral graft for reconstruction of the scaphoid proximal pole. The patients had a mean postoperative follow-up of 24 months. The mean age at the time of surgery was 30 years. Outcome measurements included total active range of wrist motion arc, grip strength, and wrist function score. We also evaluated the progression of osteoarthritis and changes in carpal height.
UNASSIGNED: No complications occurred at the donor site. The range of motion improved from 82° to 95° before and after surgery. Grip strength improved from 22 kg to 33 kg before and after surgery. There was a remarkable improvement in the modified wrist function scores of Green and O\'Brien from 40 points to 70 points before and after surgery. No progression of arthrosis was seen on the radiographs of all the patients. There was no significant difference in the carpal height ratio before and after surgery.
UNASSIGNED: Proximal scaphoid fractures may require reconstruction of the articular surfaces of the radius, capitate, and lunate. Reconstruction with a rib osteochondral graft is flexible, easy to fabricate, and can reconstruct the three articular surfaces.

Avascular necrosis of the scaphoid, often referred to as Preiser\'s disease, is little known despite the scaphoid being the second most frequently involved location in avascular pathology of the carpal bones after the lunate (Kienböck\'s disease). Nonetheless, very few cases have been reported in the medical literature over the last century. Its pathophysiology is not completely elucidated although the unique vascularization of the scaphoid and several risk factors seem to be recurrently incriminated. Two new classifications based on modern imaging have appeared in the last decade and are now considered essential supplements to Herbert and Lanzetta\'s original radiographic classification. Because of the lack of formal treatment guidelines, a wide range of different treatments have been explored over time, contributing to the confusion around this pathology. Adding to this confusion, are the numerous terms used to designate the condition and lack of knowledge concerning its pathophysiology, risk factors, clinical and radiographic presentation. The aim of this review is therefore to explore and clarify Preiser\'s disease in terms of history, terminology, pathophysiology, clinical considerations and imaging and to propose a simple updated treatment algorithm based on the results provided by a thorough review of literature (53 publications, 170 patients) since Georg Preiser\'s original and controversial description in 1910.

There is no evidence-based treatment protocol for Preiser\'s disease. This case report studies seven cases treated by pronator quadratus pedicled bone graft. Three years after the operation, all patients had good or excellent results. This technique is advocated for stage 2 Preiser\'s disease.

In 1910, Georg Preiser (1876-1913) described five cases of rarifying osteitis. Based on his imaging studies, he diagnosed post-traumatic avascular necrosis (AVN) of the scaphoid without any sign of primary fracture. This was followed by an article in 1911 in which Preiser related his findings to Kienböck\'s disease and Köhler\'s disease of the tarsal navicular. Upon searching the literature, we found descriptions and discussions of Preiser\'s imaging; however, the original images have never been published. We reproduce Preiser\'s original imaging in this current review. All of these appear to show a fracture and no signs of AVN, suggesting that Georg Preiser misinterpreted his findings. There is no apparent uniformity in the literature regarding the definition, description, or aetiology of Preiser\'s disease, and it is for this reason that we find the use of eponyms to be confusing.