If there is doubt about the interpretation of the x-ray, stress x-rays, tomograms or CT scan may be used for confirmation. Cause
The reasons for non-union are
avascular necrosis (the blood supply was interrupted by the fracture)
the two ends are not apposed (that is, they are not next to each other)
infection (particularly osteomyelitis)
the fracture is not fixed (that is, the two ends are still mobile)
soft-tissue imposition (there is muscle or ligament covering the broken ends and preventing them from touching each other)

Risk factors
Related to the person:
Age: Common in old age
Nutritional status : poor
Habits : Nicotine and alcohol consumption
Metabolic disturbance : Hyperparathyroidism
Can be found in those with NF1
Genetic predisposition
Causes related to fracture:
Related to the fracture site
Soft tissue interposition
Bone loss at the fracture
Infection
Loss of blood supply
Damage of surrounding muscles
Related to treatment
Inadequate reduction
Insufficient immobilization
Improperly applied fixation devices. Types of Nonunion
There are typically three types of nonunion described. Hypertrophic nonunion
In a hypertrophic nonunion, the fracture site contains adequate blood supply but the fracture ends fail to heal together. X-rays show abundant callus formation. This type of nonunion is thought to occur when the body has adequate biology, such as stem cells and blood supply, but inadequate stability, meaning the bone ends are moving too much. Typically, the treatment consists of increasing stability of the fracture site with surgical implants. Atrophic nonunion
In an atrophic nonunion, x-rays show little to no callus formation. This is usually due to impaired bony healing, for example due to vascular causes (e.g. impaired blood supply to the bone fragments) or metabolic causes (e.g. diabetes or smoking).
Ogden syndrome, also known as N-terminal acetyltransferase deficiency (NATD), is an X-linked disorder of infancy comprising a distinct combination of distinctive craniofacial features producing an aged appearance, growth failure, hypotonia, global developmental delays, cryptorchidism, and spontaneous cardiac arrhythmias. The first family was identified in Ogden, Utah, with five affected boys in two generations of family members. A mutation was identified as a c.109T>C (p.Ser37Pro) variant in NAA10, a gene encoding the catalytic subunit of the major human N-terminal acetyltransferase enzyme system (NatA). This same mutation was identified in a second unrelated family, with three affected boys in two generations. This severe genetic disorder has provisionally been named Ogden syndrome, as this is the city where the first affected family resides. Signs and symptoms
This is an X-linked condition affecting males more than females and is characterized by postnatal growth failure with developmental delays and dysmorphic features characterized by wrinkled forehead, anterior and posterior fontanels, prominent eyes, large down-slanting palpebral fissures, thickened or hooded eyelids, large ears, flared nares, hypoplastic alae nasi, short columella, protruding upper lip, and microretrognathia. There is also delayed closing of fontanelle, and the boys also have broad great toes. Skin is characterized by redundancy or laxity with minimal subcutaneous fat, cutaneous capillary malformations, and very fine hair and eyebrows. Death resulted from cardiogenic shock following arrhythmia, which was noted in all affected individuals. The boys had heart rhythm abnormalities and craniofacial abnormalities, which accounted for their similar appearance.