BONE PATHOLOGY

1. BONE PATHOLOGY

2. The Skeletal System • Parts of the skeletal system • Bones (skeleton) • Joints • Cartilages • Ligaments (bone to bone)(tendon=bone to muscle) • Divided into two divisions • Axial skeleton • Appendicular skeleton – limbs and girdle • The skeleton has 206 bones

3. Functions of Bones • Support of the body • Protection of soft organs • Movement due to attached skeletal muscles • Storage of minerals and fats • Blood cell formation

4. Normal bone

6. Types of Bone Cells • Osteocytes • Mature bone cells • Osteoblasts • Bone-forming cells • Osteoclasts • Bone-destroying cells • Break down bone matrix for remodeling and release of calcium • Bone remodeling is a process in which both osteoblasts and osteoclasts participate

8. Bone Fractures • A break in a bone • Types of bone fractures • Closed (simple) fracture – break that does not penetrate the skin • Open (compound) fracture – broken bone penetrates through the skin • Bone fractures are treated by reduction and immobilization • Realignment of the bone

9. Stages in the Healing of a Bone Fracture Slide 5.19

10. Stages in the Healing of a Bone Fracture 1-Haematoma formation 2-Fibrocartilage callus formation 3-Boney callus formation 4-Bone remodelling Slide 5.19

11. Classification of Bone Pathology: Infectious Diseases of Bone Developmental Disorders of Bone Metabolic Disorders of Bone Avascular Bone Necrosis (Osteonecrosis) Paget’s Disease of Bone Tumors of Bone

12. Infectious Diseases of Bone Osteomyelitis Pott’s Disease

13. OSTEOMYELITIS Classification: • Non- bacterial osteomyelitis: • Viral osteomyelitis • Sarcoidosis • Radiation osteomyelitis Definition: This is inflammation of bone and bone marrow

14. Bacterial osteomyelitis: • Acute suppurative osteomyelitis • Acute haematogenous osteomyelitis • Acute non-haematogenous osteomyelitis • Chronic osteomyelitis: • Chronic non-specific osteomyelitis • Chronic specific osteomyelitis ( TB & Syphilis)

15. ACUTE HAEMATOGENIUS OSTEOMYELITIS • Haematogenous osteomyelitis is predominantly seen in children and involves the highly vascular long bones especially those of the lower limbs. • In adults, haematogenous spread is more common to the lumbar vertebral bodies than elsewhere. Definition: Acute osteomyelitis is an acute inflammation of bone caused by an infecting organism

16. Pathogenesis The spread of infection is usually haematogenous. 1-Among children: the metaphysis of the long bones is the most common site, where blood flow slows in the sinusoids, allowing bacteria to adhere to the vascular membranes. 2-Local trauma with skin penetration and seeding of organisms is another pathway. 3-Localized trauma without skin penetration to the bone causing haematoma, vascular obstruction in the metaphyseal region and bacteraemia at around the same time result in infection.

18. Metapheseal blood sinsoids

19. Stages of disease 1-Inflammation: Initial inflammation with vascular congestion and increased intra-osseous pressure. 2-Suppuration: Pus within the bones forces its way through the Haversian system and forms a subperiosteal abscess in 2-3 days.

20. 3-Sequestrum:Vascular obstruction and infective thrombus decrease or obstruct the periosteal and endosteal blood supply, causing bone necrosis and sequestrum formation in approximately 7 days. 4-Involucrum:This is new bone formation from the stripped surface of periosteum. 5-Resolution or progression to complications: With antibiotics and surgical treatment early in the course of disease, osteomyelitis resolves without any complications.

21. MP of acute osteomyelitis Inflammation of bone

22. Acute osteomyelitis

23. Complications of osteomyelitis: Pathologicalfracture Spread of infection: eg. Arthritis (joint inflammation), myositis (muscle inflammation) or neuritis (nerve inflammation) Blood spread: causing toxaemia & septicaemia Chronic suppurative osteomyelitis: including sequestrum formation and skin sinus formation Damage to the growth plate causing subsequent growth deformity

24. Pott's disease Pott's disease is a presentation of extra pulmonary tuberculosis that affects the spine, a kind of tuberculous arthritis of the intervertebral joints. The lower thoracic and upper lumbar vertebrae are the areas of the spine most often affected.

25. Pott’s Disease

26. Tuberculosis of the spine in an Egyptian mummy

27. Clinical presentation: Back pain Fever Night sweating Anorexia Weight loss Spinal mass, sometimes associated with numbness, paraesthesia or muscle weakness of the legs

28. Diagnosis Blood tests – elevated erythrocyte sedimentation rate (ESR) Tuberculin skin test Radiographs of the spine Bone scan CT of the spine Bone biopsy MRI

29. Pott’s Disease; X-ray Pott’s Disease; MRI

30. Complications Vertebral collapse resulting in kyphosis Spinal cord compression Sinus formation Paraplegia (called Pott's paraplegia)

31. Tuberculous in long bones • Commonly around the knee, affects metaphysis and epiphysis, rarely diaphysis • Well-defined lytic area

32. Tuberculous arthritis • The hip and knee are the most commonly affected peripheral joints. • Characterized by joint space narrowing and erosions which may lead to extensive destruction of the articular cortex.

33. HEREDITARY BONE DISORDERS Achondroplasia Osteogenesis imperfecta osteopetrosis

34. Achondroplasia • Clinically: • Long bones are short and thick  short extremities dwarfism • Cranial and vertebral bone spared  relatively large head and trunk • Normal intelligence, life span and reproductive ability

35. Achondroplasia

36. Osteogenesis imperfecta 1-Generalized osteopenia: brittle bones, resulting in recurrent fractures and skeletal deformity 2-Most patients have an abnormally thin sclera with blue hue Abnormally thin sclera with blue hue

37. Laxity of joint ligments leads to hypermobilty • Involvement of the bones of the inner and middle ear produces deafness • Some patients have dentinogenesis imperfecta: small, fragile and discolored teeth due to deficiency of dentin • The skin may be abnormally thin and the skin is susceptible to easy bruising

38. Laxity of joint ligaments Osteogenesis imperfecta Brittle bones

39. Dentinogenesisimperfecta

40. Osteopetrosis • Marble bone • Hereditary defect leading to thick sclerotic bones Pathology: -Increased bone density and thickening of bone cortex -The thickened bones are brittle and fracture easily

41. X-ray findings: • Symmetrically generalized osteosclerosis • Long bones may have broadened metaphyses, resulting in an "Erlenmeyer flask" deformity

42. Osteopetrosis X-ray findings • Symmetrically generalized • Osteosclerosis • Long bones may have broadened • metaphyses, resulting in an • "Erlenmeyer flask" deformity Osteosclerosis Erlenmeyer flask shaped deformity

43. Metabolic Diseases of Bone

44. Osteoporosis • Occurs due to: • Loss of organic bone matrix and minerals. • Resulting in : • Decreased bone mass and density. • Decreased thickness of cortical and trabecular bone. • Refers to increased porosityof skeleton. • Osteoporotic bones: • Thin and fragile and are susceptible to fracture.

45. Osteoporotic vertebral body Normal Vertebral body

46. Fracture Osteoporosis

47. Types of Osteoporosis • Localized : e.g. disuse of a limb • Generalized: involves entire skeleton. • Primary: • Old age (Senile) • Estrogen deficiency (postmenopausal) • Secondary: (due to underlying disease) • Cushing’s disease (Hypercortisolism) • Drugs (Heparin and Steroids)

48. Postmenopausal Osteoporosis Due to estrogen deficiency Estrogen deficiency  increased resorption of bone by osteoclasts and decreased formation of bone by osteoblasts.

49. Genetic factors Nutrition Physical activity Peak bone mass • Menopause • ↓ estrogen • ↑ osteoclast activity • Aging • ↓ activity of osteoblasts • ↓ physical activity Osteoporosis

50. Clinical findings: • Bone pain • Weight bearing bones predisposed to • Compression of vertebral bodies (most common) • Colles’ fracture of distal radius. • Fracture femoral neck. • Loss of height and kyphosis