Pathologic Bone Fracture

A pathological bone fracture is a bone fracture which occurs without adequate trauma and is caused
by a preexistent pathological bone lesion. It also occurs when a bone breaks in an area that was
already weakened by another disease. Include resorption of bone mass (osteoporosis), reduction
of bone quality (osteomalacia, osteonecrosis), insufficient bone production (osteogenesis
imperfecta, fibrous dysplasia), augmented bone resorption (giant cell granulomas, aneurysmal
bone cyst), pathological bone remodelling (Paget's disease), or local bone destructionoe due to
tumorous growths.A pathological bone fracture has to be detected clinically as well as
radiologically and its cause diagnosed histologically in order to ensure adequate therapy.
Osteochondral fractures

Osteochondral fractures of the lower extremities are important injuries because they can cause pain
and dysfunction and often lead to osteoarthritis. An osteochondral fracture is considered an injury
that damages the cartilage and underlying subchondral bone. Osteochondral/chondral fractures are
related to trauma and may present acutely. However, they are often initially missed, being
misdiagnosed as a pure soft tissue injury, and present as chronic lesions. Most of the literature to
date focuses on chronic lesions and potential strategies to stimulate repair or regeneration of
cartilage.

Physeal fractures

Physeal fractures also called Salter-Harris fractures are important childhood fractures that involve
the physis. They are relatively common and important to differentiate from other injuries because
the involvement of the physis growth plate may cause premature closure resulting in limb
shortening and abnormal growth. The fracture plane was usually contained within the physis but
could involve many regions of the physis. In some instances, the fracture plane extended to the
physeal epiphyseal borde., When the fracture extended through the physis to the epiphyseal
physeal border, there was greater physeal disorganization and formation of vertical septa leading
to physeal bars. Physeal bars appeared to form at sites of vertical fibrotic septa into which marrow
cells, osteoclasts, and osteoblasts had migrated. Bar formation mediated by primary osteogenesis
rather than by endochondral bone formation followed.

Avulsion Fractures

Avulsion fracture is considered a special type of fracture. Repetitive muscle contraction or a violent
muscle contraction may pull off a fragment of cortical and medullary bone across the tendon
insertion that has a stronger tensile strength than the bone. Common sites of involvement are ischial
tuberosity (ischial apophyseolysis), at the insertion of the hamstring muscles; inferior pubic ramus,
at the insertion of the adductor muscles; and iliac spine, at the insertion of the rectus femoris. The
radiographic picture commonly shows extensive reactive bone proliferation and may suggest
malignant neoplasms. Intense uptake of technetium in bone scan. The histological pattern is similar
to a repairing fracture process – endosteal and periosteal callus.

FISSURE FRACTURE

Cracks or fissure lines will occur when direct trauma is applied to any long or flat bone. Generally
the fissures are formed in one cortex of the bone and are covered by an intact periosteum. Bones
may have single or multiple fissure lines of any configuration: transverse, oblique, spiral,
longitudinal, or radiating from a central point. Since fissure fractures occur only in a single cortex
and represent an incomplete fracture, the fractured bone should maintain its normal shape.
Inflammation

 Hematoma forms and provides source of hemopoieitic cells capable of secreting growth
factors.
 Macrophages, neutrophils and platelets release several cytokines
 this includes PDGF, TNF-Alpha, TGF-Beta, IL-1,6, 10,12
 they may be detected as early as 24 hours post injury
 lack of TNF-Alpha (ie. HIV) results in delay of both
enchondral/intramembranous ossification
 Fibroblasts and mesenchymal cells migrate to fracture site and granulation tissue forms
around fracture ends
 during fracture healing granulation tissue tolerates the greatest strain before
failure
 Osteoblasts and fibroblasts proliferate
 inhibition of COX-2 (ie NSAIDs) causes repression of runx-2/osterix, which are critical
for differentiation of osteoblastic cells

Bone Production

 Primary callus forms within two weeks. If the bone ends are not touching, then bridging
soft callus forms.
 the mechanical environment drives differentiation of either osteoblastic (stable
enviroment) or chondryocytic (unstable environment) lineages of cells.
  Enchondral ossification converts soft callus to hard callus (woven bone). Medullary
callus also supplements the bridging soft callus
 cytokines drive chondocytic differentiation.
 cartilage production provides provisional stabilization
 Type II collagen (cartilage) is produced early in fracture healing and then followed by
type I collagen (bone) expression.
 Amount of callus is inversely proportional to extent of immobilization
 primary cortical healing occurs with rigid immobilization (ie. compression plating)
 enchondral healing with periosteal bridging occurs with closed treatment

Bone Remodeling

 Begins in middle of repair phase and continues long after clinical union
o chondrocytes undergo terminal differentiation
o complex interplay of signaling pathways including, indian hedgehog (Ihh),
parathyroid hormone related peptide (PTHrP), FGF and BMP
o these molecules are also involved in terminal differentiation of the appendicular
skeleton
 type X collagen types is expressed by hypertrophic chondrocytes as the extraarticular
matrix undergoes calcification
 proteases degrade the extracellular matrix
o cartilaginous calcification takes place at the junction between the maturing
chondrocytes and newly forming bone
 multiple factors are expressed as bone is formed including BMPs, TGF-Betas, IGFs,
osteocalcin, collagen I, V and XI
o subsequently, chondrocytes become apoptotic and VEGF production leads to new
vessel invasion
o newly formed bone (woven bone) is remodeling via organized
osteoblastic/osteoclastic activity
 Shaped through
o Wolff's law: bone remodels in response to mechanical stress
 o piezoelectic charges : bone remodels is response to electric charges: compression
side is electronegative and stimulates osteoblast formation, tension side is
electropostive and simulates osteoclasts

References

Kerr R, Forrester DM, Kingston S. Magnetic resonance imaging of foot and ankle trauma.
Orthop Clin North Am 1990;21:591–603.

Barrie H.J. Osteochondritis dissecans 1887-1987. A centennial look at König’s memorable

phrase. J. Bone Joint Surg. Br. 1987;69(5):693–695.

Aiyer, A. ( 28 April 2018) Fracture Healing. Retrieved from

https://www.orthobullets.com/basic-science/9009/fracture-healing

Bone Healing( n.d) Retrieved from https://www.foothealthfacts.org/conditions/bone-healing

Milgram J. Tangential osteochondral fracture of the patella. J Bone Joint Surg Am. 1943;25:271–
280.