BONES AND JOINTS

Bone is a specialised connective tissue which has

structural ,protective,metabolic and
haemopoietic function.attachment of muscles &
tendons,movement.
Regions :Epiphysis, metaphysis ,Diaphysis.
Types of bone: 1.Compact Or Cortical
2.Cancellous Or spongy –red marrow
Cells of bone tissue: Osteoblasts,Osteocytes &
Osteoclasts
Osteoid –unmineralised matrix
Ossification: 1.membranous 2.Endochondral
 Bone fracture & healing
 Fracture—Discontinuity of the bone,
Types;simple,compound, pathological
 Phases: 1.inflammatory phase -haemorrahge-
inflammatory cells-granulation tissue-non-
lamellar or woven bone--soft tissue callus
 2.Reparative Phase- soft tissue callus replaced
by Lamellar bone and is mineralised.3weeks
weight bearing can be tolerated.
 3. Remodelling Phase.-Osteoclasts
 Process of healing takes 6-8 weeks
 Complications:non
union,Pseudoarthrosis,deformity
 Osteoporosis
 Reduced bone mass leading to porosity of
bones –more resorption of bone than
formation.
 -Primary: Postmenopausal, old age ( oestrogen
, anabolic steroid effect reducing )
 Secondary:1.Hyperthyroidism
2.Hyperparathyroidism.3. Drugs-steroids
 4.malabsorption ,malnutrition.
 Complications : patholgical fracture.
 Osteomyelits
 Inflammation of the bone and marrow
 Types: 1.Pyogenic 2.tuberculous
 Pyogenic Osteomyelitis :80-90%
Staphylococcus aureus-10-20%
Esch.coli,pseudomonas,klebsiella,haemophilus
 Portal of entry; 1.skin –compound fracture
 2. tooth abscess –maxilla,mandible
 3.Blood borne : boil & paranychia
 4. surgical procedure:
 Osteomyelits-pathogenesis
 Metaphysis -capillary loops-slowing of blood
 Organism reaches marrow
 Acute inflammatory reaction( exudate formed )
 Necrosis of bone due to pressure & pus
formation ( Sequestrum).
 Pus penetrates periosteum & skin to form
draining sinus
 Reactive New Bone
( Involcrum)formationaround the periphery of
inflammatory reaction
 Osteomyelitis - Pyogenic
 Complications ;1.Septecemia 2.acute
suppurative arthritis 3.Pathological fracture
 4.squamous cell carcinoma 5.Amyloidosis
 Clinical features.-fever,chills,malaise, pain at
site
 Diagnosis : .1.Radiological
 2.blood culture 3. biopsy
 Tuberculous Osteomyelitis
 Mycobacterium tuberculosis
 Source : Blood borne from a focus of pulmonary
or extrapulmonary disease
 Site : spine ( thoracic & Lumbar vertebra ) Pott’s
abscess.caseous necrosis with giant cells
 Clinical features :low grade evening rise of
temp.pain on movement,weight loss
 Complications:1.destruction of vertebra2.Psoas
abscess 3. TB arthritis
Bone tumours-Osteogenic sarcoma
 Most common, highly malignant of bone tumours.
Characterised by formation of bone matrix or
osteoid ( unmineralised bone ) by malignant cells.
 Age /sex :10-20 years, Boys more affected.
 Site: arises from Metaphysis of long bones of
extremities- Lower end of femur,upper tibia,upper
fibula,proximal humerus.
 Osteogenic sarcoma-Morphology
 Gross: big ,bulky,grey-white in colour,gritty.
 Shows areas of haemorrhage & cystic
degeneration .tumour extends into the adjacent
soft tissue ( Mutton leg appearance )
 Microscopy : pleomorphic tumour cells with
large hyperchromatic nuclei & show mitotic
figures.Bizarre tumour giant cells are common.
 Production of Osteoid by malignant tumour
cells is the diagnostic feature.
 Osteogenic sarcoma ( contd )
 Clinical features :painful,progressively
enlarging mass around the knee or other
involved site. The area is swollen and
tender.the adjacent joint function is affected.
 Radiographic : Codman Triangle-space
between cortex and elevated periosteum
appears as a triangular shadow. Sun-Ray –
parallel lines of mineral deposition in the
periosteum.
 Spread: Local ; Blood spread –lungs,brain
 Joints
 Joints formed by two or more bones provide
movements and mechanical stability to the
body. The joints consist of articular cartilage
with a joint space ( synovial cavity ) lined by
synovial membrane. The articular cartilage
provides friction free movement within the
joints and acts as a shock absorber. The
synovial cavity contains clear & viscous
synovial fluid containing hyaluronic acid.The
fluid acts as a lubricant & supplies nutrient to
the articular hyaline cartilage.
 Joints

 1.Fibrous Joints: no movement-skull,maxilla

 2.Cartilaginous Joints : slight movement

 Symphysis Pubis & bodies of vertebra

 3. Synovial joints : Free movement

 Osteoarthritis
 Osteoarthritis is a degenerative ,slowly
progressive, non-inflammatory joint disease.
 Osteoarthritis is a misnomer as there is no
inflammatory reaction: Osteoarthosis will be a
better term.
 Involves articular cartilage & subchondral bone.
 Joints affected; weight bearing –knee,hips,spine
Non-weight bearing-inter-phalangeal joints of
fingers,first carpometacarpal&tarsometatarsal
 Osteoarthritis
1. Primary :aging process
2. Secondary:younger individuals-
a) previous injury to a joint b) diabetes
c)haemochromatosis
Pathogenesis & morphology :
Changes in the articular cartilage; cracks develop
on the surface of articular cartilage-synovial
fluid flows along these cracks & penetrates
deeper into the cartilage.Dead pieces of
cartilage fragment are shed as loose
bodies(Joint mices)into the synovial cavity.
 Osteoarthritis
 Changes in the subchondral bone: After the
articular cartilage is sloughed off, the bone
beneath it ( subchondral bone) is exposed &
becomes the new articular surface. The bone
appears thick,smooth,shiny giving it polished
ivory appearance ( bone eburnation). Synovial
fluid enters bone marrow forming subchondral
bone cyst. The loculated fluid collection
increases in size surrounded by reactive bone
wall.Mushroom-shaped pearly-grayish bony
outgrowths(spurs) called Osteophytes develop
in the periphery of the joint surface.
 Osteoarthritis
 Clinical features:
 Slowly progressive disease & causes long-
term disability
 Deep aching pain which worsens with joint
movement & is relieved by rest.
 Joint swollen, tender & may demonstrate
crepitus
 Osteophytes in spine can cause nerve root
compression.
 Heberden nodes-osteophytes in distal
interphalangeal joints
 Rheumatoid Arthritis
 Rheumatoid arthritis is a chronic ,progressive,
 Inflammatory,Autoimmune disease.It is a
systemic disorder where inflammatory changes
not only affect the joints but also blood vessels,
heart,skin.Antigen-antibody complexes are
found in the blood& synovial fluid. Genetic
factors may be involved.
 RA is an acute febrile condition usually with
periods of remission & exacerbation of varying
lengths of time.
 Rheumatoid arthritis
 Most commonly affects proximal
interphalangeal & metacarpophalangeal
joints.other jts: feet,elbow,knee,ankle,spine.
 With each febrile exacerbation,there is
additional & cumulative damage to the joints
leading to increasing deformity,pain and loss of
function.
 Age/Sex; 40-70 years– Women more affected
Rheumatoid Arthritis- Morphology
 Synovium: Gross : Involved synovium is oedematous and thickened.
 Microscopy:1.Synovial hyperplasia which may form finger-like

structures(villi).
 2.dense inflammatory infiltrate of lympocytes

Plasma cells & Macrophages.

3.Pannus formation-pannus consists of inflammatory cells,granulation

tissue and synovial stroma.Pannus grows over articular cartilage&

destroys it.It bridges the apposing bones forming a Fibrous Ankylosis

which may ossify to form a Bony Ankylosis.

 Rheumatoid Arthritis
 Clinical Features: slow and insidious in onset.
Presents with malaise,fatigue,fever. The
affected joints are swollen,warm,painful and
stiff on arising or following inactivity.
 Deformities:radial deviation of the wrist,ulnar
deviation of the fingers,flexion-hyperextension
abnormalities of the fingers(swan neck )
 Laboratory findings: 1.Rheumatoid
factor2.Anti-CCP( cyclic citrullinated peptide )
3.antinuclear antibody 4. ESR . 5. CRP
 Gouty Arthritis
 Gout is characterised by hyperuricemia and deposition
of urate crystals in joints & kidneys.
 Disorder of Purine metabolism.
 Classification :1. Primary ( idiopathic) hyperuricemia
occurs without any disease.
 2.secondary :a) Increased catabolism of nucleic acid due
to increased cell turnover-leukemia, cancer b)
decreased excretion of uric acid with normal production.
( eg. Chronic renal failure)
 Gouty Arthritis
 Uric acid is the end-product of purine metabolism.
Gouty arthritis is usually an extremely painful
attack with a rapid onset of inflammation.The
iflammation is precipitated by the deposition of uric
acid crystals in the synovium & fluid within the
joint.The white cells engulf the crystals& release
chemicals which promote inflammation which
causes pain,heat & redness of the joint.
 Diet rich in purine : meat, fish
 Gouty Arthritis-Morphology
Acute arthritis : characterised by oedema, congestion and
dense infiltration of synovium by neutrophils.MSU
( monosodium urate)crystals are long,needle shaped and
arranged in small clusters in the synovium.

Chronic tophaceous arthritis:It follows repeated attacks of

acuteattacks.The synovium shows fibrosis,thickening and
infiltration by inflammatory cells.It forms a pannus which
destroys the articular cartilage and triggers juxta-articular
bone erosion.
 Gouty Arthritis
Tophi ; lesions consisting of large aggregates of
monosodium urate (MSU) crystals,surrounded by
inflammatory cells .They are pathognomic of gout
and are commonly found in the articular
cartilage,periarticular ligaments, tendons & soft
tissues.Microscopically they consist of aggregates
of MSU surrounded by macrophages,lympocytes
and foreign body giant cells.
 Gouty Arthritis
 Clinical features:1. common in men than
women
 2. age : after 30 years 3. commonest site--- Big
Toe—other sites:ankle,heel& wrist
 4. Four stages-a) asymptomatic hperuricemia
 b)acute gouty arthritis c)intercritical gout
 d)chronic tophoceous gout. Initial acute attack
resolves completely followed by asymptomatic
interval( intercritical).Recurrent attacks lead to
deformity.5.high serum uric acid & presence of
uric acid crystals in the synovial fluid .