SKELETAL SYSTEM pathology nursing ppt.pptx

skeletal system pathology

1. SKELETAL SYSTEM

2. FRACTURE HEALING: Healing of fracture by callus formation depends upon some clinical considerations whether the fracture is: traumatic (in previously normal bone), or pathological (in previously diseased bone); complete or incomplete like green-stick fracture; and simple (closed), comminuted (splintering of bone), or compound (communicating to skin surface).

3. Primary union of fractures occurs when the ends of fracture are approximated surgically by application of compression clamps or metal plates. In these cases, bony union takes place with formation of medullary callus without periosteal callus formation. The patient can be made ambulatory early but there is more extensive bone necrosis and slow healing. Secondary union is more common form of fracture healing when the plaster casts are applied for immobilisation of a fracture. Though it is a continuous process, secondary bone union is described under the following 3 headings: i ) Procallus formation ii) Osseous callus formation iii) Remodelling

4. I. PROCALLUS FORMATION 1. Haematoma formation 2. Local inflammatory response 3. Ingrowth of granulation tissue 4. Callus composed of woven bone and cartilage II. OSSEOUS CALLUS FORMATION The procallus acts as scaffolding on which osseous callus composed of lamellar bone is formed. The woven bone is cleared away by incoming osteoclasts and the calcified cartilage disintegrates.

5. III. REMODELLING During the formation of lamellar bone, osteoblastic laying and osteoclastic removal are taking place remodelling the united bone ends, which after sometime, is indistinguishable from normal bone. The external callus is cleared away, compact bone (cortex) is formed in place of intermediate callus and the bone marrow cavity develops in internal callus .

6. Complications of Fracture Healing 1. Fibrous union may result instead of osseous union if the immobilisation of fractured bone is not done. Occasionally, a false joint may develop at the fracture site (pseudo-arthrosis). 2. Non-union may result if some soft tissue is interposed between the fractured ends. 3. Delayed union may occur from causes of delayed wound healing in general such as infection, inadequate blood supply, poor nutrition, movement and old age.

7. OSTEOMYELITIS An infection of the bone is termed osteomyelitis (myelo = marrow). A number of systemic infectious diseases may spread to the bone such as enteric fever, actinomycosis, mycetoma (madura foot), syphilis, tuberculosis and brucellosis. Types - pyogenic osteomyelitis and tuberculous osteomyelitis.

8. Pyogenic Osteomyelitis Pyogenic or suppurative osteomyelitis is usually caused by bacterial infection and rarely by fungi. H aematogenous route, most commonly in the long bones of infants and young children (5-15 years of age) E tiologic agent - Staphylococcus aureus , streptococci, Escherichia coli, Pseudomonas, Klebsiella and anaerobes Clinically, the child with acute haematogenous osteomyelitis has painful and tender limb. Fever, malaise and leucocytosis generally accompany the bony lesion. Radiologic examination confirms the bony destruction.

9. MORPHOLOGIC FEATURES : Depending upon the duration, osteomyelitis may be acute, subacute or chronic. The basic pathologic changes in any stage of osteomyelitis are: suppuration, ischaemic necrosis, healing by fibrosis and bony repair. The sequence of pathologic changes is as under: The infection begins in the metaphyseal end of the marrow cavity which is largely occupied by pus. At this stage, microscopy reveals congestion, oedema and an exudate of neutrophils. The tension in the marrow cavity is increased due to pus and results in spread of infection along the marrow cavity, into the endosteum, and into the haversian and Volkmann’s canal, causing periosteitis. The infection may reach the subperiosteal space forming subperiosteal abscesses. It may penetrate through the cortex creating draining skin sinus tracts.

10. 4. Combination of suppuration and impaired blood supply to the cortical bone results in erosion, thinning and infarction necrosis of the cortex called sequestrum. 5. With passage of time, there is formation of new bone beneath the periosteum present over the infected bone. This forms an encasing sheath around the necrosed bone and is known as involucrum. Involucrum has irregular surface and has perforations through which discharging sinus tracts pass. 6. Long continued neo-osteogenesis gives rise to dense sclerotic pattern of osteomyelitis called chronic sclerosing nonsuppurative osteomyelitis of Garré . 7. Occasionally, acute osteomyelitis may be contained to a localised area and walled off by fibrous tissue and granulation tissue. This is termed Brodie’s abscess. 8. In vertebral pyogenic osteomyelitis , infection begins from the disc (discitis) and spreads to involve the vertebral bodies

11. Tuberculous Osteomyelitis MORPHOLOGIC FEATURES C entral caseation necrosis surrounded by tuberculous granulation tissue and fragments of necrotic bone. The tuberculous lesions appear as a focus of bone destruction and replacement of the affected tissue by caseous material and formation of multiple discharging sinuses through the soft tissues and skin. Involvement of joint spaces and intervertebral disc are frequent.

12. Tuberculosis of the spine, Pott’s disease, often commences in the vertebral body and may be associated with compression fractures and destruction of intervertebral discs, producing permanent damage and paraplegia. Extension of caseous material along with pus from the lumbar vertebrae to the sheaths of psoas muscle produces psoas abscess or lumbar cold abscess . The cold abscess may burst through the skin and form sinus. Long-standing cases may develop systemic amyloidosis.

13. OSTEOPOROSIS

14. Osteoporosis or osteopenia is a common clinical syndrome involving multiple bones in which there is quantitative reduction of bone tissue mass but the bone tissue mass is otherwise normal. This reduction in bone mass results in fragile skeleton associated with increased risk of fractures and consequent pain and deformity. The condition is common in elderly people and more frequent in postmenopausal women. The condition may remain asymptomatic or may cause only backache. M ore extensive involvement is associated with fractures, particularly of distal radius, femoral neck and vertebral bodies.

15. Levels of serum calcium, inorganic phosphorus and alkaline phosphatase are usually within normal limits. Many non-invasive techniques are now available for measurement of bone mass e.g. DEXA and SEXA scans (dual energy and single-energy X-ray absorptiometry), quantitative CT and ultrasound. PATHOGENESIS Primary osteoporosis results primarily from osteopenia without an underlying disease or medication. Primary osteoporosis is further subdivided into 2 types: idiopathic type found in the young and juveniles and is less frequent, and involutional type seen in postmenopausal women and ageing individuals and is more common . The exact mechanism of primary osteoporosis is not known but there is a suggestion that it is the result of an excessive osteoclastic resorption and slow bone formation

16. RISK FACTORS 1. Genetic factors- more marked in whites and Asians than blacks. 2. Sex - more frequent in females than in males. 3. Reduced physical activity - as in old age. 4. Deficiency of sex hormones - oestrogen deficiency in women as in postmenopausal osteoporosis and androgen deficiency in men. 5. Combined deficiency of calcitonin and oestrogen. 6. Hyperparathyroidism. 7. Deficiency of vitamin D. 8. Local factors - which may stimulate osteoclastic resorption or slow osteoblastic bone formation.

17. Secondary osteoporosis is attributed to a number of factors and conditions (e.g. immobilisation, chronic anaemia, acromegaly, hepatic disease, hyperparathyroidism, hypogonadism, thyrotoxicosis and starvation), or as an effect of medication (e.g. hypercortisonism , administration of anticonvulsant drugs and large dose of heparin). MORPHOLOGIC FEATURES Except disuse or immobilisation osteoporosis which is localised to the affected limb, other forms of osteoporosis have systemic skeletal distribution. Most commonly encountered osteoporotic fractures are: vertebral crush fracture, femoral neck fracture and wrist fracture. There is enlargement of the medullary cavity and thinning of the cortex.

18. Histologically, osteoporosis may be active or inactive type. Active osteoporosis is characterised by increased bone resorption and formation i.e. accelerated turnover. There is an increase in the number of osteoclasts with increased resorptive surface as well as increased quantity of osteoid with increased osteoblastic surfaces. The width of osteoid seams is normal. Inactive osteoporosis has the features of minimal bone formation and reduced resorptive activity i.e. reduced turnover. Histological changes of inactive osteoporosis include decreased number of osteoclasts with decreased resorptive surfaces, and normal or reduced amount of osteoid with decreased osteoblastic surface. The width of osteoid seams is usually reduced or may be normal.

19. OSTEOARTHRITIS

20. Osteoarthritis (OA), also called osteoarthrosis or degenerative joint disease (DJD), is the most common form of chronic disorder of synovial joints. Primary OA - wear and tear with repeated minor trauma, heredity, obesity, ageing. Occurs in elderly. Secondary OA - previous wear and tear phenomena involving the joint such as previous injury, fracture, inflammation, loose bodies and congenital dislocation of the hip. Occurs at any age.

21. MORPHOLOGIC FEATURES W eight-bearing joints such as hips, knee and vertebrae are most commonly involved but interphalangeal joints of fingers may also be affected. The pathologic changes occur in the articular cartilages, adjacent bones and synovium 1. Articular cartilages - there is loss of cartilaginous matrix (proteoglycans). followed by focal loss of chondrocytes, and at other places, proliferation of chondrocytes forming clusters. loosening, flaking and fissuring of the articular cartilage resulting in breaking off of pieces of cartilage exposing subchondral bone. Radiologically, this progressive loss of cartilage is apparent as narrowed joint space

22. 2. Bone - The denuded subchondral bone appears like polished ivory. There is death of superficial osteocytes and increased osteoclastic activity causing rarefaction, microcyst formation. The margins of the joints respond to cartilage damage by osteophyte or spur formation. Loosened and fragmented osteophytes may form free ‘joint mice’ or loose bodies. 3. Synovium. in advanced cases there is low-grade chronic synovitis and villous hypertrophy. There may be some amount of synovial effusion associated with chronic synovitis.