pathology bone disorders Flashcards
what is bone
it is a rigid inflexible mineralised connective tissue
what is the ECM of bone mineralised by
ca/PO salts
why do we need bone
structural purposes
metabolic
what structural purposes do we need bone for
physical integrity
protection of squishy organs
insertion of muscles and tendons
what is haematopoiesis
The formation development and maturation of blood cells
Happens in the bone marrow (majority) and the liver for adults
where does haematopoesis occur in embryos
the yolk sac
what is bone made from
one is the non cellular mineralised matriculates
cellular component
what composes the non cellular mineralised material
type 1 collagen
calcium hydroxyapatite crystals
regulatory proteins and Growth factors
what is type 1 collagen called int he context of bone
osteoid
what is the cellular component of bone
osteoblasts
osteocytes
osteoclasts
stem cells which give rise to the osteoblasts
what do osteoblasts do
they form the bone matrix
mesenchymal in origin
secretory function and secrete the osteoid
involved in mineralisation
what do osteocytes do
entrapped osteoblasts which are inactive
what do osteoclasts do
from the macrophage lineage
sit at the surface of the bone and take place in bone resorption
how can we group different types of bone
by maturity
by location
what are the different types of bone which vary by maturity
woven bone
lamellar bone
describe woven bone
immature bone where the bone is laid down very quickly by osteoblasts
later remodelled to lamellar bone
more chance of fracturing
describe lamellar bone
bone is laid down in parallel bands
normal healthy bone
what are the 2 types of lamellar bone
compact bone
cancellous/trebecular bone
which type of bone is most immature
woven bone
what are the different types of bone which vary by location
cortical
cancellous
describe the bone remodelling cycle
activation resorptions reversal formation termination
what happens in the activation stage of bone remodelling
we need hormones or damage to activate the osteoblasts
OBs secrete cytokines
osteoclasts start to secret substances that break down the bone
what happens in the resorptions phase of bone remodelling
macrophage lineage osteoclasts secrete substances that resorp the bone
the the osteoclasts migrate
what happens in the removal phase of bone remodelling
monocytes clear debris for the bone formation
what happens in the formation phase of bone remodelling
the osteoblasts are recruited
they secrete a new matrix which is mineralised
OBs now sit on new bone and some incorporated as osteocytes
what is osteoarthritis
progressive erosion of articular cartilage
it is not just erosion but a complex impbalance of damage and repair
what can we see in osteoarthritis
the underlying bone becoming exposed and then leading to cysts and pain
what is the common symptom of osteoarthritis
joint space narrowing
Pain and functional limitation
Morning stiffness
what are the common signs of osteoarthritis
Crepitus( crunching)
Restricted movements
Bony enlargement
Instability
what are the primary causes of osteoarthritis
unknown causes
what is the secondary causes of osteoarthritis
pre existing joint disease eg RA, gout
metabolic disease eg acromegaly
systemic disease eg haemophilia
what are the investigations we can do for osteoarthritis
blood tests
erythrocyte sedimentation rate
CRP- c reactive protein
rheumatoid factor is NEGATIVE
what is the management of osteoarthritis
hydrotherapy, weight loss
NSAIDS
joint replacement
describe RA
It is an autoimmune disease
resulting in inflammation of the synovialm of the joints but can be systemic and affect the lungs
risk factors for RA
women more likely
strong association with the HLA antigen
assoc with epstein barr virus
can also occur due to contribution of the oral microbiome
how does RA cause damage in the body
occurs from a process called citrullination of self antigens- changes in self antigens and they are recognised as abnormal and the immune system attacks them
what happens to the synovial cavity
becomes hyper cellular which leads to inflammation and damage
what is pannus formations
inflammatory infiltrate forming a mass in the tissues
what are some systemic manifestations of RA
carpal tunnel syndrome
pericarditis
lymphadenopathy
sjogrens syndrome
investigations for RA
CRP
anti citrullinated peptide antibodies
rheumatoid factor +
management for RA
no cure
NSAIDS
disease modifying anti rheumatic drugs
what is ankylosis
abnormal stiffening in joints due to bony fusion
describe pagets disease
It Is a disorder of bone turnover/remodelling
There is increased osteoclastic bone resorption and increase of new bone formation
Increased formation > resorption but it is woven bone
what is the aetiology of pagets disease
unknown
but
can be viral/microbial
genetic history
symptoms of pagets disease
bone and joint pain
cotton wool skull appearance
hypercementosis
high alkaline + phosphate levels
what are the phases of pagets disease
hot
mixed
cold
what is the hot phase of pagets disease
high osteoclast activity
what is the mixed phase of pagets disease
There is a little bit of osteoblast activity as well as osteoclast activity
what is the cold phase of pagets disease
inactive burn out phase
treatment for pagets disease and osteoporosis
bisphosphonates
what do bisphosphonates do
inhibit osteoclast activity and recruitment
what is the issue with bisphosphonates
need to be careful of BRONJ bisphosphonate related osteonecrosis of the jaw
describe osteomyelitis
→ It is inflammation of the bone or bone marrow
→ Usually always due to infection
how can we get osteomyelitis
through blood stream
extension from the adj site
direct implantation of the organisms
what bacterium is the most common cause of osteomyelitis
S aureus
what is the clinical presentation of osteomyelitis
○ Fever
○ Localised bone pain
○ Overlying tenderness/erythema
○ Hard to diagnose so we can use a bone biopsy
treatment of osteomyelitis
immobilise
antibiotics
maybe drainage
why might we get osteomyelitis of the jae
Polymicrobial
Odontogenic infection
why might people get tuberculous osteomyelitis
Haematogenous spread from reactivated primary TB focus
what are the subtypes of osteomyelitis
focal sclerosis
diffuse scleorising
proliferative periostitis
what are the types of fracture
simple compound comminuted displaced stress greenstick pathologic
what is the phases of fracture healing
- inflammatory phase
- reparative phase
- remodelling phase
what happens in the inflammatory phase
1st week
Haematoma forms- source of hemopoietic cells and growth factor
Macrophages, neutrophils and platelets release Cytokines
Fibroblasts come to the fracture site
Granulation tissue forms around the fracture ends
Neovascularisation
Osteoblasts, chondrocytes( lay down cartilage) and fibroblasts leading to callus forming
what happens in the endochondral phase
Cartilage provides provisional stabilisation
Endochondral ossification converts soft callus to hard callus woven bone
what happens in the remodelling phase
The hard woven bone is remodelled into lamellar bone
describe osteonecrosis
infarction of the bone marrow
why does osteonecrosis occur
due to
alcohol
steroids
fracture
what is the underlying cause of osteonecrosis
vascular insufficiency due to mechanical injury to the blood vessel eg thromboembolism
presentations of osteonecrosis
→ Joint pain shoulder or hip
→ Can be asymptomatic–> collapse of articular bone
MRI shows bone marrow oedema
management of osteonecrosis
→ Symptomatic
→ Surgical decompression
→ Grafts
joint replacement
what happens if we have a drop in the calcium serum levels
PT glands to secrete PTH which increases calcium by
→ Increased osteoclast bone resorption
→ Increased calcium intestinal absorption
→ Increased synthesis of 1.25- dihydroxy vitamin D3
→ Increased renal tubular resorption Ca
→ Increased renal excretion PO4
what happens when we have low calcium levels
bone resorption increases
what is the other name for rickets
osteomalacia
describe osteomalacia
The osteoid has not been mineralised and therefore defective mineralisation of the epiphyseal plate in children leading to weakened bones
what is rickets
osteomalacia in children
what is the aetiology of rickets
Aetiology is anything that interferes with bone mineralisation
Eg deficient intake or absorption of vitamin D( nutritional, malabsorption
Renal failure
Inhibitors of mineralisation
Defective vitamin D receptors
what are the dental complications of vitamin D deficiency
Familial hypophosphatemia Large pulp chamber Thin enamel Dentinal defects which is globular Prone to abscesses
what is hyperparathyroidism
Anything pathological which causes increase in PTH
what does an increase of PTH do
→ Osteoclast bone resorption → Intestinal Ca absorption → synthesis of 1.25- dihydroxy vitamin D3 → renal tubular resorption Ca → renal excretion PO4
what are the different types of hyperthyroidism
primary hyperthyroidism
secondary
tertiary hyperthyroidism
what is the most common cause of asymptomatic hypercalcaemia
primary hyperthyroidism
caused by adenoma, hyperplasia, malignancy
what are the symptoms of hyperthyroidism
bones, stones, groans and moans
Bones- disease and pain
Stones- renal stones
Groans- GI groans including constipation nausea, gallstones and pancreatitis
Moans- CNS alterations, depression, lethargy
describe osteogenesis imperfecta
brittle bone disease
what are the gene mutations for osteogenesis imperfecta
COL1A1
COL1A2
dental manifestations of osteogenesis imperfecta
Dentinogenesis imperfecta type II
In OI type IB
Blue discoloured teeth
what is endochondral ossification
Cartilage is used as a template and is replaced by bone
what is intramembranous ossification
In the skull, maxilla and mandible they are formed by the deposition of bone within primitive mesenchymal tissue
what are the craniofacial issues with bone growth and achondroplasia
→ Macrocephaly → Flattened nasal bridge → Hypoplasia of midfacial structures → Maxillary hypoplasia → Relative overgrowth of the mandible → Narrowing of anterior plate Orthodontic intervention
