Metabolic bone diseases

Management And PT Implications

 Your Assignment
 Read a scientific paper and present a resume/summary, in no more
than a page (500 words)
 Related to orthopaedics or orthopaedic PT
 Last 5 years
 Open access journal, conference, academic essay…
 Sent to us via Email, no handwriting.
 Title
 Introduction
 Material
 Methods
 Results
 Discussion
 Conclusion
 General bone diseases
metabolic and endocrinal diseases
• The main bone functions, support,
protection and leverage, deal carefully
with diseased bones…
• Normal control of mineral content (and
bone composition)
• Bones as mineral reservoir, which
constitutes around 50% of the total bone
mass
• The continuous flux of minerals to and
from bones mediated by local factors
and hormones and implemented by
cellular activity
Normal bone structure
 Normal bone structure
• Stages of bone formation:
Osteoid= the unmineralised
bone
Woven bones= newly
formed bones
Lamellar bones= mature
bones
• Types of lamellar bones:
1. Cortical (compact) bones
2. Cancellous bones,
 Normal bone structure
• The cotical bone:
Dense and strong, found where
support matters, as in shafts of long
bones and the subchondral plates
Arranged in osteons (haversian
systems) containing haversian canals
having bd vessels and lymphatics
and surrounded by densly packed
concectric lamellae of bone.
Haversian canals are connected to
both the periosteal and endosteal
surfaces by the small Volkmann’s
canals
 Normal bone structure
• The cancellous bone
More porous, found near long bone
ends and in the vertebrae, made
up of trabeculae in sheets like
honey comb appearance and
arranged according to the
mechanical needs. Being weaker,
the effects of metabolic diseases
appear 1st in trabecular bones
 Normal bone structure
• Blood supply to bones is really
rich. Vessels in the Haversian
canals form an anastomotic
network between the
medullary and periosteal blood
supply.
• Periosteal coverage and
enosteal lining occur in fully
formed bones. The deepest
layer of the former is a bone
forming layer besides its blood
supply role
 Normal bone structure
• Bone cells and its functions:
Osteoblasts are cocerned with
bone formation and
osteclast activation
Osteoclasts are concerned with
bone resorption
Osteocytes are concerned with
communication and
providing information about
stresses
 Bone development and growth
• Endochondral ossification, increasing mainly
length
 Bone development and growth
• Intramembranous
ossification
increasing mainly
width
• Bone modelling and
remodeling
 Normal bone structure
• Wolff’s law, intensity increases for areas of
stress
• Age related changes in bones for men and
women
 Mineral exchange and Ca metabolism
• Bone turnover and mineral exchange, new bone
replaces old bone throughout life
• Ca metabolism, daily intake, absorption and
excretion, and the factors affecting that process.
• Phosphorous and vitamin D
• PTH, the fine regulator of Ca metabolism
• Calcitonin, the counterpart of PTH
Mineral exchange and Ca metabolism
 Mineral exchange and Ca metabolism
• Other factors controlling Ca metabolism:
1. Estrogen
2. Adrenal corticosteroids
3. Local factors like insulin-like growth factor,
transforming growth factor, interleukin-1
prostaglandins and bone morphogenetic proteins
4. Mechanical factors like loss of wt, lack of exercise,
ms weakness prolonged bed rest and limb
immobilization = osteoporosis
 Metabolic bone diseases
• Depletion of bone tissue manifested as:
1. Quantitative diminution of bone mass,
osteoporosis
2. Poorly mineralised osteoid, osteomalacia
3. Excessive bone resorption and increased PTH,
osteitis fibrosa
Beware while dealing with diseased bones
 Metabolic bone diseases
• Common feature is the bad quality bones, be
very careful while doing physiotherapy for
those pts
• General clinical assessment
• Measurement of bone mass
• Biochemical testing
 Osteoporosis
• Osteoporosis is quantitative loss of bone mass
• Osteopenia and osteoporosis
• Postmenopausal osteoporosis, high and low
turnover osteoporosis
• Risk factors for osteoporosis, like white race, family
history, early onset menopause, early hysterectomy,
lack of exercise and smoking and alcohol
 Osteoporosis
Clinical picture:
Back pain and
generalised bone aches,
kyphos deformity, history
of fractures.
X ray shows diminished
bone density as well as
DEXA scan
 Osteoporosis
• Prevention and treatment
Identify high risk groups, DEXA screening, adequate
Ca and vit D intake, stop smoking and alcohol
1. Hormonal replacement, many side effects
2. Bisphosphonates, best R modality now
3. Denosumab, newer approach
4. Management of fractures accordingly
 Osteoporosis
• Secondary osteoporosis
1. Hypercortisonim
2. Thyrotoxicosis
3. Alcohol abuse
4. Multiple myeloma and carcinomatosis
5. Disuse
6. Others, like rheumatoid arthritis
 Rickets and osteomalacia
• Inadequate mineralization of bone
• Deformed joints and widened metaphysis in
children
• Soft indentable and easy fracturing bones in adults
 Vitamin D deficiency rickets
• Used to be common in cold
areas(no sun rays)
• Clinically:
1. Craniotabes
2. Cupping(broadening) of the
epiphyses, distal radius, ankles
for physeal overgrowth
3. Rachitic rosary
4. Lateral indentation of the
chest(Harrison’s sulcus)
 Vitamin D deficiency rickets
• X ray: thickening and widening of the
epiphyses, distortion of the metaphyses and
bow legs
 Vitamin D deficiency rickets
• Biochemical investigations:
1. Serum ca and p and 25 HCC low
2. Alkaline phosphatase high
3. Urinary ca excretion low
• Treatment: vitamin D administration+ ca
supplement
 Osteomalacia
• Defects anywhere in the metabolic pathway of
vitamin D
• Clinical picture insidious bone pains or ms
weakness probably for years, may present
with a stress fracture or insufficiency fracture
(to minor traumatic incidents).
• X ray generalized rarefaction, old poorly heald
fractures
Osteomalacia
 Osteomalacia
• Investigations: as in rickets
• Biopsy may be needed
• After diagnosis of osteomalacia, we re-
investigate to know the cause, like
malabsorption synd, liver or kidney disease…
• Treatment :
Treatment of the cause
Supplementation with sufficient doses of Ca and
vitamin D
 Hyperparathyroidism
• Over secretion of
parathormone
hormone from the
parathyroid gld
• Occurs 1ry, 2ry or
trtiary
• The cardinal feature is
elevated serum Ca and
parathyroid hormone
 Hyperparathyroidism
pathology
• Ca absorption from the intestines as well as
Ca reabsorption from the kidneys are both
increased
• Ca is mobilised out of its bone storage
excessively leading to adverse effects on the
bones in the form of rarefaction and porosis
and on the kidneys in the form of stones,
nephrocalcinosis, infections
• Soft tissue calcifications can occur elsewhere
 Hyperparathyroidism
pathology
• In severe cases, bones have cystic changes
and fibrous replacement, osteitis fibrosa
cystica
• Hge and giant cell reaction within the fibrous
stroma may give rise to brownish tu. Like
masses whose liquification leads to fluid filled
cysts, brown tu.
 Hyperparathyroidism
C/P
• Middle aged females
• Symptoms of hypercalcaemia like anorexia, N&V,
abdominal pains, depression, fatigue and ms
weakness.
• Symptoms of renal disease
• Chondrocalcinosis
• Bone pains and pathological fractures
• X rays:
Subperiosteal cortical
resorption of the
middle phalanges is
most pathognomonic
generalised
osteoporosis
Vertebral collapse
Cortical erosions and
cyst formation
• Lab work:
Elevated s. Ca and PTH
and reduced s. P
 Hyperparathyroidism
Treatment
• Conservative in mild
cases, adequate
hydration and decrease
Ca intake
• Treatment of associated
pathological fractures if
any
• Operative in severe
cases,
parathyroidectomy
Osteits fibrosa cystica
 Renal osteodystrophy
• Bone weakness associated
with chronic renal disease
• Elevated s. P, and
defective vit D metabolism
leads to diminished s. Ca
• Children more affected,
stunted growth
• Treatment of renal dis vit
D replacement, then
correctin of deformitirs
 Scurvy
• Defeciency of vit C leads to defective collagen and
consequently defective osteid formation
• Results in bone weakness and bleeding tendency
• X ray shows marked porotic changes, the ring sign
• Treatment is by vit C replacement
 Paget’s disease
• Enlarged and thickened
bones with brittle internal
architecture
• Prevalent in the west and
reason is unknown
• Stage of resorption
(vascular), liable for
deformities and stage of
excess formation, liable for
pathological fractures
 Paget’s disease
c/p
• More in older age
• Common in pelvis and tibia
• May remain dormant for many
years
• Deformities of the spine and the
legs give the classic picture
• Occasional dull and constant
pains
• Commonly present with
pathological fractures
• X ray appearance is characteristic.
• S. alkaline phosphatase raised
while s Ca and P are normal
 Paget’s disease
complications
• Fractures
• Nerve compression
• Malignant transformation
into osteosarcoma
• Hypercalcaemia
• Cardiac failure
 Paget’s disease
Treatment
• Treatment : antiresorptive
medicines like calcitonin and
bisphosphonates for symptomatic
pts.
• ORIF for fractures ”not an easy job”
• Surgical excision for ostesarcoma
(prognosis is bad)
Endocrine • The endocrine system has
disorders direct effect of growth and
maintenance of the skeletal
system
• Hypopituitarism in childhood
leads to obesity and
weakness of the physes,
slipping of the proximal
epiphysis while in adults
leads to osteoporosis
• Hyperthyroidism may give
rise to porotic manifestations.
 Hypercortisonism
• Hypercortisonism (cushing’s
syndrome) excess secretion of
glucocorticoids leads to
porotic manifestations of
bones by stimulating bone
resorption and inhibiting
bone formation.
• Delayed healing, little
purchase for internal fixation
devices, high infection
incidence and avascular
necrosis are important
features of the disease
 Hypercortisonism
• Treatment with corisone
has the same effects
• Ca and vit D supplements
may improve the condition