Pathologic Fracture

Yudha Mathan Sakti

Sub Bagian Orthopaedi dan Traumatologi

RS DR Sardjito - FK Universitas gadjah Mada
 Spaceflight Osteopenia

• Characteristic of bone loss that occurs during spaceflight

• Lost an average of > 1% bone mass per month spent in space

• Weightlessness during space flight results in increases urinary

calcium excretion, decreases intestinal calcium absorption,
and increases serum calcium level  Bone loss

If you don’t use it you will lose it !!!

 Patophysiology

• After peak bone mass  bone loss occurs :

– Rate of 0.3 percent per year in men
– 0.5 percent per year in women

and INCREASES

2 to 3 percent per year at the onset of

menopause
(an 8 per cent decrease in trabecular bone and a 0.5 per cent decrease in cortical bone)

Instructional Course Lectures, The American

Academy of Orthopaedic Surgeons - Osteoporosis:
Diagnosis and Treatment*†
Instructional Course Lecture
An Instructional Course Lecture, The American
4
Academy of Orthopaedic Surgeons
 Wolff’s Law
• The principle that states :

‘every change in the form and the function of a bone or in the

function of the bone alone, leads to changes in its internal
architecture and in its external form’

• Bone remodels in response to mechanical stress in order to

maintain constant strain energy per bone mass throughout

• it grows more dense in areas experiencing high stress, while

resorbing density in areas experiencing low stress

To survive the stress it has to be strong (survival property)

With the courtesy of Rahadyan Magetsari
Gadjah Mada University

Compare the medial and lateral cortex

Mechanical Properties of Bone
With the courtesy of Rahadyan Magetsari
Gadjah Mada University
 Definition

• A pathologic fracture is one that occurs when the

normal integrity and strength of bone have been
compromised by invasive disease or destructive
processes.

• Bone is broken, through an area, weakened by pre-

existing disease, by a degree of stress, that would
have left the normal bone intact.

Koval, Kenneth J.; Zuckerman, Joseph D. Title: Handbook of Fractures, 3rd Edition, 2006 Lippincott
Williams & Wilkins
 Etiology
Any condition that will decrease the strucctural integrity of bone

• Congenital defect of bone (Osteogenesis imperfecta)

• Disorder of cartilage growth (Achondroplasia, multiple exostosis,
dyschondroplasia, etc)
• Nutritional and vitamin deficiencies (Rickets)
• Hormonal imbalance (Hyperparathyroidism, cortisone treatment)
• Atrophic conditions (Disuse osteoporosis, senile osteoporosis)
• Infection (osteomyelitis)
• Primary and metastasis bone tumour
 Pathophysiology

Etiologic
factor of Inadequate
peak bone Low bone
decrease mass/
bone mass
impaired
density bone
Decrease
quality Fractures
in bone
mass/bone
quality
Calcium/
vitamin D Trauma
deficiency
 Pathophysiology
More active Vitamin D Parathyroid Calcitonin Estrogen Cortico Exercise
Bone Cells (PTH) steroid
Bone Osteoblast
Formation
↑ ↓ ↑ ↑ ↓ ↑
Bone Osteoclast
Absorption
↓ ↑ ↓ ↓ ↑ ↓
Function Act as couple Creates absorption decrease estrogen increase Bone
Ca of calcium the receptors Ca formed in
binding across the number are present excretion the area in
protein gut, bone and in calcium need
resorption, activity osteoblast- and block (Wolff’s
increased of osteo like cells Resorp tion law)
retention on clasts in the gut
kidneys

Heaney, R. P.; Recker, R. R.; and Saville, P.

D.: Menopausal changes in bone remodelling.
J. Lab. and Clin.
12
 How to diagnose?
• History

• Physical examination

• Supporting examination

Be sistematic and assess the possible etiology

 MECHANISM OF INJURY

• Trivial trauma or even during normal activities

• Pain at the site of fracture prior to injury

• A history of multiple fractures

• Predisposing history of osteopenia (possible comorbid)

• Risk factors such as smoking or environmental exposure

to carcinogens
 Physical examination
• Principle : Look, Feel, Move

• standard physical examination for fracture diagnosis

• attention of a possible soft tissue mass at fracture site

• evidence of primary disease such as lymphadenopathy,

thyroid nodules, breast masses, prostate nodules, rectal
lesions

• examination of other painful regions to rule out

impending fractures
 Rickets
• Rickets is the softening and weakening of bones in children,
usually because of an extreme and prolonged vitamin D deficiency.

• Serum calcium may show low levels of calcium, serum phosphorus

may be low, and serum alkaline phosphatase may be high from
bones or changes in the shape or structure of the bones.

• Hypotheses of Environment mismatch :

• Northern latitudes have selection for lighter skin that allows UV
rays to produce Vitamin D. Conversely, latitudes near the equator
have selection for darker skin that can block the majority of UV
radiation to protect from toxic levels of Vitamin D, as well as skin
cancer

• Nutritional rickets VS vitamin D resistant rickets

 Vitamin D
Vitamin D activation

Precursor Vit D
Photolysis reaction
The Sun Skin Food / Supplement
(7-Dehidrokolesterol)

1, 25, dihydroxyvitamin D
Liver Kidney
25, hydroxyvitamin D
2 nd Activation
↑ ↑ 1 ά hidroksilase

Active Vitamin D
(Absorb Calcium in Gastrointestinal tract)
Parathyroid hormone

17
 Osteogenesis imperfecta

• Defective connective tissue disease (because of a

deficiency of Type-I collagen synthesis)

• As a genetic disorder, OI has historically been viewed

as an autosomal dominant disorder of type I
collagen.

• Most cases have been caused by mutations in the

COL1A1 and COL1A2 genes.
 Bone
With the courtesy of Rahadyan Magetsari
Gadjah Mada University

Without Mineral Without Collagen

Osteogenesis imperfecta
 Hyperparathyroidism

• Disease results from excessive secretion of

parathyroid hormone either due to solitary (50-85%)
or multiple (10%) adenomas, hyperplasia (10-40%), or
rarely due to a carcinoma of a single parathyroid gland.

• Primary hyperparathyroidism is usually diagnosed as a

result of chance finding of raised serum calcium or
complications associated with hypercalcemia such as
polyuria, polydipsia, muscle weakness, gastrointestinal
upsets and renal stone formation.

• Associated with brown tumour

Senile osteoporosis
 Patophysiology

• After peak bone mass  bone loss occurs :

– Rate of 0.3 percent per year in men
– 0.5 percent per year in women

and INCREASES

2 to 3 percent per year at the onset of

menopause
(an 8 per cent decrease in trabecular bone and a 0.5 per cent decrease in cortical bone)

Instructional Course Lectures, The American

Academy of Orthopaedic Surgeons - Osteoporosis:
Diagnosis and Treatment*†
Instructional Course Lecture
An Instructional Course Lecture, The American
25
Academy of Orthopaedic Surgeons
Patophysiology

Why Women?
26
OPG is an essential mediator for Osteoclast
inhibition
Estrogen (17 β Estradiol)

Osteoclast Formation, Function,

and Survival Inhibited

4/19/2019 27 9
Normal Osteoporosis
Morphologic changes due to aging

29
 Metastasis Bone Disease (MBD)

• History, especially of thyroid, breast, or

prostate nodule
• Review of systems, especially gastrointestinal
symptoms, weight loss, flank pain, hematuria
• Physical examination, especially lymph nodes,
thyroid, breast, abdomen, prostate, testicles,
and rectum
 Metastasis Bone Disease (MBD)

• The skeleton is one of the commonest sites of secondary

cancer; in patients over 50 years bone metastases are seen
more frequently than all primary malignant bone tumours
together.

• The commonest source is carcinoma of the breast; next in

frequency are carcinomas of the prostate, kidney, lung,
thyroid, bladder and gastrointestinal tract.

• The commonest sites for bone metastases are the vertebrae,

pelvis, the proximal half of the femur and the humerus.
 Metastasis Bone Disease (MBD)

• Spread is usually via the blood stream; occasionally, visceral

tumours spread directly to adjacent bones (e.g. the pelvis or
ribs).

• Metastases are usually osteolytic, and pathological fractures

are common.

• Bone resorption is due either to the direct action of tumour

cells or to tumour-derived factors that stimulate osteoclastic
activity.
 TREATMENT

Initial Treatment
• Standard fracture care: reduction and immobilization
• Evaluation of underlying pathologic process
• Optimization of medical condition

Nonoperative Treatment
• In general, fractures through primary benign lesions of bone
will heal without surgical management.
• Healing time is slower than in normal bone, particularly after
radiation therapy and chemotherapy
 TREATMENT
Operative Treatment

• Goals of surgical intervention are:

– Pain relief
– Mechanical support for weakened or fractured bone to
permit the patient to perform daily activities.
– Decreased length and cost of hospitalization.
 F, 43 y.o
Chief of complaint: Pain on the left hip
 Diagnosis :
Close pathologic fracture of subtrochanter of the left femur
due to suspected MBD (breast cancer)
 M, 12 y.o
Diagnosis : Close pathologic fracture of middle third of the right tibia due to
susp fibrous dysplasia
Before op 1 month after op

9 months after op
Clinical condition 9 months after op
Thank you ^^