Pathology Flashcards
1
Q
How can pathologies assist the FoAn?
A
- Where multiple individuals share very similar biological profiles, pathology or past trauma may be the key identifying factor. The rarer the pathology, the better.
- If the pathology is the result of trauma, medical records may exist and can be compared to remains to aid in identification.
2
Q
Challenges of skeletal pathologies
A
- Must be able to distinguish between pathology, trauma, and taphonomic processes. Plants (roots) and animals may cause holes etc. which mimic disease.
- Bone has very limited responses to disease = build up or break down. Many diseases will have similar appearances > differential diagnosis.
- Incomplete skeletons may make diagnosis difficult if key discerning elements are not present.
- Must determine how the pathology affected the individual in life, how it will have manifested to those around them > this is the identifying factor.
3
Q
Affect of pathology on bio profile
A
- Ancestry: pathologies may manifest differently in differing populations, being more prevalent or severe in certain ancestral groups which may aid in ancestry estimation.
- Sex: Osteoarthritis may obscure pelvic morphology limiting its use in sex estimation.
- Age: Bone diseases such as osteoporosis and osteoarthritis cause degenerative changes, causing the skeleton to appear older than it is.
- Stature: Certain pathologies may affect bone length or disrupt bone growth (osteomalacia or rickets).
4
Q
what does presence of skeletal lesions indicate?
A
- Severe stress > good immunity > chronic ill health > bone reacts resulting in observable changes > individual dies (possibly unrelated) . pathology evident on bone.
- Skeletal pathologies are likely to represent the healthier individuals as they lived with and fought disease for a significant period of time.
5
Q
What does absence of skeletal lesions indicate?
A
- Absence of evidence is not the evidence of absence. Bone is often the last structure to respond to disease = no skeletal lesions simply mean the disease killed the individual before affecting the bone.
- severe stress > poor immunity > bone has no time to react > person dies > no changes observed.
- Could mean individual was perfectly healthy and died of accidental causes.
6
Q
Bone response to disease
A
- Bone formation by osteoblasts.
- Bone resorption by osteoclasts.
- Mixed bone response = both involved.
- Lytic lesions: osteoclast activity greater than osteoblast = bone destruction.
- Blastic lesions: osteoblasts greater than osteoclast = increased bone formation + density.
7
Q
Periostitis (non-specific)
A
- Inflammation of periosteum leads to increased blood supply and bone formation > eventual remodelling.
- Woven bone forms rapidly and poorly attached, colour of soil.
- Compact lamellar bone will form over time; organised, striated structure: forms slowly due to chronic conditions or healing of woven bone.
8
Q
Osteitis (non-specific)
A
- Inflammation of bone substance = increased formation/thickening.
- Decreased diameter of medullary cavity = remodelling occurs.
9
Q
Osteomyelitis (non-specific)
A
- Bone infections: medullary cavity, cortical bone; local or diffuse; acute or chronic.
- Cause resorption or formation and cloaca formation.
- Caused by: direct open fractures, local soft tissue spread, blood borne infections.
- May cause sequestrum formation = isolated bone segment or involucrum = sheath around cortical bone.
- Soft tissue indication = fistula/sinus forms as drainage channel for infection.
10
Q
Reactive arthropathies (non-specific)
A
- Joint degeneration or fusion as a result of infection.
- Can be septic arthritis or Reiter’s syndrome.
- Septic arthritis = infection spreads from blood to joints, bacteria enter synovium and joint capsule causing inflammation and destroying cartilage = erodes joint surface = ankylosis/fusion occurs if untreated.
11
Q
Tuberculosis (specific)
A
- Caused by mycobacterium.
- Acute or chronic.
- Blood borne or via direct contact.
- Lytic lesions affect ribs and spine.
- Septic arthritis + ankylosis cause collapse of vertebral bodies due to destructive lesions = Pott’s Kyphosis.
- On the rise in vulnerable populations: preventable and treatable.
12
Q
Syphilis (specific)
A
- Treponemal bacterial disease
- Venereal or congenital.
- Venereal causes distinctive lesions on cranial vault = Caries sicca
- Tertiary syphilis: chronic and multifocal = sclerotic lesion formation as a result of bone formation or destruction. Rhino-maxillary bone resorption may occur
13
Q
Charcot’s joint (specific)
A
- Peripheral neurotrophic arthropathy: a secondary condition which results from infectious disease. Loss of peripheral nerve function can be caused by neurosyphilis or type 2 diabetes.
- Ankylosis of the joint caused by repeated trauma due to individual being unaware or unable to prevent it.
14
Q
Anaemia (nutritional and metabolic)
A
- Lack of/low RBC cause marrow to expand in an effort to resupply = widening of medullary cavity, cortical thinning, widening metaphyses.
- Porotic Hyperostosis: symmetrical lesions on the frontal and parietal bones; thickening and coarsening of diploe with a loss of outer cortical surface = porosity
- Cribra orbitalia: similar to PH but limited to orbital roof.
- Argued that low iron levels prohibit erythropoiesis so cannot be the cause of PH or CO.
15
Q
Vitamin D deficiency (nutritional and metabolic)
A
- Maintains blood calcium levels, lack causes rickets or osteomalacia.
- Caused by lack of sunlight or inadequate nutrition.
3.In children: cartilage ossification centres fail to calcify which restricts cartilage proliferation, stunting growth = failure to create an adequate precursor for bone. - Bones will be malformed and shortened with flaring, may cause scoliosis and thinning of cranial elements.
- osteomalacia = bowing of weight baring elements.
