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Weber-Cech Classification of Non-Union and Delayed Union of Bones

Judet and later Muller, Weber, Cech, etc. classified non-union or pseudoarthrosis into two types:


The first type is characterized by vascular proliferation or hypertrophy at the fracture ends, with a significant biological response; Vascular-rich non-union (hypertrophic), the fracture ends are vital and show a significant biological response. Studies using Strontium-85 show that the blood supply to the fracture ends is abundant. This type can be further divided into the following subtypes:


① “Elephant foot” type (hyperplastic callus non-union): The fracture ends show hypertrophy and abundant callus, while simultaneously, the fracture ends become sclerotic, and the marrow is blocked by the sclerotic bone. The fracture ends are viable, and this type of non-union has a strong ability for new bone formation. This is mainly due to inadequate stabilization after fracture reduction, insufficient immobilization, or premature weight-bearing.


② “Hoof” type (sclerotic non-union): The fracture ends show sclerosis, mild hypertrophy, and little or no external callus formation. This is mainly due to insufficient stability from plates and screws. This is the most common type of non-union after surgery. Some callus formation occurs at the fracture ends but is insufficient to connect them; at this stage, the fracture ends still retain the ability for repair.


③ Nutritional deficiency type (avascular non-union): The fracture ends are of a non-hypertrophic type, lacking callus. This mainly occurs when the fracture ends are significantly displaced, separated, or misaligned during internal fixation. There is a gap at the fracture ends, and no callus or sclerosis is generated at any time.




The second type is characterized by ischemia or atrophy of the fracture ends, lacking biological response.

Ischemic (atrophic) non-union, the fracture ends lack vitality and show a minimal biological response. Studies using Strontium-85 show poor blood supply to the fracture ends.


Ischemic non-union can be classified into the following subtypes:


① Twisting wedge non-union: Characterized by a piece of bone between the two fracture ends that lacks or has no blood supply, which can heal with one end but not with the other. This is mainly seen in tibial fractures fixed with plates and screws. Sometimes also seen in multifragmentary femoral fractures.


② Comminuted non-union: Characterized by the presence of one or more necrotic bone fragments, X-rays show no callus formation. This mainly occurs when the plate fails in the fixation of acute fractures. Typically involves a third fracture with no blood supply.


③ Defect non-union: Characterized by a defect in the bone shaft, where the fracture ends are vital but cannot connect across the defect, leading to atrophy over time. This mainly occurs in open fractures, secondary osteomyelitis, or due to tumor resection of parts of the bone shaft. Bridging the defect requires large bone grafting or the application of the Ilizarov technique.


④ Atrophic non-union: This type has a missing segment of bone, with the defect filled by scar tissue lacking osteogenic potential, leading to atrophy, osteoporosis, and thinning of the fracture ends, with a wide fracture gap and bone end necrosis. This type of non-union in adults is often due to severe bone necrosis caused by significant injury, especially with massive necrosis of the periosteum. This type is referred to as “avascular non-union,” where the ability to form bone is completely lost.




To assess the repair capacity of the fracture ends and the presence of biological activity, bone scanning is useful. Generally speaking, the elephant foot type (hyperplastic callus type) and hoof type (sclerotic type) of non-union show strong RI accumulation at the fracture ends and the gap, and even in the avascular type (nutritional deficiency type), there is still considerable RI accumulation, while complete absence of RI accumulation at the fracture ends is rare. In atrophic (avascular) types, the accumulation of RI is very weak and may sometimes be absent. Therefore, although bone scanning cannot fully confirm the timing of treatment, strong RI accumulation can indicate biological repair capacity, which can be classified as delayed union rather than non-union. Very low accumulation can be classified as non-union, which is useful for selecting treatment methods, particularly in assessing the necessity of autologous cancellous bone grafting.



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