Non Union

While a well-accepted definition remains elusive, a nonunion can be understood broadly as

failure of fracture healing. The rate of nonunion varies depending on which bone is involved
and several other injury specific and patient-specific factors.132 For instance, scaphoid
fractures suffer from an increased rate of nonunion, believed to be mostly related to the tenuous
blood supply that is often damaged at the time of injury. Additionally, numerous patient-
specific factors including smoking, obesity, nutritional status (e.g., vitamin D deficiency), and
several medications have been associated with healing failure. A high percentage of patients
with an otherwise unexplained nonunion, who underwent appropriate management, where later
found to have at least one endocrine abnormality.

Nonunions are usually divided into two subcategories. These are atrophic nonunions that
demonstrate little or no biologic healing response and hypertrophic nonunions that demonstrate
a biologic healing response but do not ultimately progress to complete union. Both are
potentially modifiable by the treating clinician, so understanding their etiology and treatment
strategies offers an avenue for possible intervention. Related conditions include delayed union,
in which appropriate healing is achieved over a prolonged time course, and malunion, in which
healing occurs but with residual deformity. All nonunions should undergo a systematic
evaluation and investigation to determine the etiology as this will dictate the appropriate
treatment.

Atrophic Nonunion

Atrophic nonunions are defined by the lack of a healing response. Despite being given
sufficient time, the fracture does not show any demonstrable signs of healing. This is typically
attributable to an underlying biologic problem. Common reasons for failure of the underlying
healing mechanisms include infection, prior radiation treatments to the injury site, and
insufficient vascular supply. However, there is no currently accepted noninvasive method to
determine which injuries will ultimately go on to nonunion. While there has been considerable
work establishing the temporal relationships of various serum markers with the various phases
of healing, there is no clear consensus for identifying an actionable marker of delayed healing.
One promising marker appears to be TGF-β1. In 10 patients with evidence of delayed healing
compared to an age-matched cohort, a finding of decreased TGF-β1 levels at 4 weeks was
highly predictive of subsequent nonunion.There is considerable interest in understanding the
initial inflammatory response to fracture and the role this plays in the healing process. It is
generally accepted that “disordered” inflammation is deleterious for fracture healing,44,47 but
there remains work to be done to elucidate precisely which cellular and molecular parameters
are critical, and therefore whether current therapies inappropriately alter these dynamics.
Whether clinical therapeutics can target these processes remains to be determined.
Correspondingly, the treatment for an atrophic nonunion is typically focused on the biologic
environment. If the cause of the underlying nonunion can be elucidated, then strategies
designed to combat that issue are typically employed. Often, bone grafting is used to foster an
improved biologic milieu. There are several considerations for this, but the gold standard
treatment involves using autologous bone graft, which has the benefit of being patient-derived
and contains viable cell populations as well as existing bone matrix to serve as a template for
repair.

Hypertrophic Nonunion

A hypertrophic nonunion shows biologic responsiveness, in many cases more robust than
normal healing, but the fracture is unable to form a complete union. Hypertrophic nonunions
most frequently occur because the mechanical environment was not suitable for healing. Often,
there is inadequate mechanical stability and the fracture callus is unable to transition to osseous
callus, which ultimately leads to an overproduction of fibrous tissue and the persistent of
hypertrophic cartilage in the callus. In these cases, it is typically not necessary to augment the
biologic capacity of the fracture site, but rather adequate stability is sufficient for appropriate
healing. The fibrous callus generally must be debrided and then improved mechanical stability
provided. This can take various operative and nonoperative forms, but most commonly it
involves open reduction and internal fixation (ORIF). As our understanding of the
transdifferentiation of hypertrophic chondrocytes to osteoblasts improves, this may represent
an opportunity for intervention to induce the transition of formed chondrocytes to osteoblasts
to drive callus maturation and remodeling.

(referensi Rockwood)

UNION, DELAYED UNION AND NON-UNION

Repair of a fracture is a continuous process : any stages into which it is divided are necessarily
arbitrary. In this chapter the terms ‘union’, ‘delayed union’ and ‘non-union’ are used, and they

are defined as follows:

• Union –

Union is incomplete repair; the ensheathing callus is calcified. Clinically, the fracture site is
painless on palpation and weight-bearing. X-rays show bridging callus. The fracture line is
completely or almost obliterated and crossed by bone trabeculae. Repair is complete and further
protection is unnecessary.

• Timetable – How long does a fracture take to unite? No precise answer is possible because
age, constitution, blood supply, type of fracture and other factors all influence the time taken.
A spiral fracture in the upper limb takes 6–8 weeks to unite; in the lower limb it needs twice as
long. Add 25% if the fracture is not spiral or if it involves the femur. Children’s fractures, of
course, join more quickly. These figures are only a rough guide; there must be clinical and
radiological evidence of consolidation before full stress is permitted without splintage.

• Delayed union –

Delayed union means that fracture healing is not taking place at the expected rate

and time but healing is still possible. Additional effort should be aimed at achieving fracture
healing as fast as possible. Clinically, the fractured limb has local swelling and movement or
partial weight-bearing is painful.

• Non-union –

Sometimes the normal process of fracture repair is thwarted and the bone fails to unite. Unless
there is bone loss, non-union is usually defined as fracture that has not healed 9 months post
operation and there is no visible progress of healing during the last 3 months. Causes of aseptic
non-union are: (1) mechanical instability or (2) impaired vascularity. Septic non-unions occur
with infected osteosynthesis. Aseptic non-unions can be either stiff or mobile as judged by
clinical examination. The mobile ones can be as free and painless as to give the impression of
a false joint (pseudoarthrosis). On X-rays, non-unions are typified by a lucent line still present
between the bone fragments; sometimes there is exuberant callus trying – but failing – to bridge
the gap (hypertrophic nonunion) or at times none at all (atrophic non-union) with a withered
appearance to the fracture ends