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Paleopathology
Midterm studying: weeks 1-5 (joint/spine/metabolic/infective disorders)
| Question | Answer |
|---|---|
| What did Rudolf Virchow & Robert Wilson Shufeldt Jr. contribute to the study of paleopathology | R.W.S.Jr. first coined the term in 1893; R.V. developed comparative pathology in the late 1800s, noting lesions in a cave bear and Neandertal similar to human conditions |
| What is the importance of the Archaeological Survey of Nubia (1907–1911) to the study of paleopathology | The first large scale, semi-fully-recorded excavation; multiple observational anatomical studies on skeletal remains |
| Why is Aleš Hrdlička (1869-1943) considered the ‘Father of Physical Anthropology’ | Founded Am.J.Phys.Anth. in 1918; provided many descriptive studies of pathology/anomaly in multiple regions of the New World; Reinforced the importance of human skeletal recovery in archaeological context for permanent study and systematic analyses |
| ‘The New Anthropology’ | (Sherwood Washburn, 1951) the holistic approach of understanding biological processes, genetics, and evolutionary adaptations in studying human populations is highly impactful |
| The two major assumptions underpin palaeopathological practice | (i) that the response of bone to pathological stimuli has not changed substantially over time (ii) that the expression of skeletal disease has also remained reasonably constant. (human skeletal response to disease has not changed over time) |
| Intramembranous Ossification | Originating from a membrane (flat bones/skull) |
| Endochondral Ossification | Originating from cartilage (most bones) |
| The bony matrix consists of: (main protein and mineral) | type I collagen and hydroxyapatite |
| Cortical/compact bone | Dense outer bone, resists torsion and impact |
| Trabecular/spongy/cancellous bone | Porous inner bone, resists compression |
| The osteon and its components (4) | The functional unit of bone; Haverisian canal (central bloo vessels), concentric lamellae (tree rings), canalculi (little transverse canals that connect osteocytes & allow exchange), osteocytes (mature bone cells residing in lancunae) |
| Osteoblasts vs osteoclasts | Blasts produce, clasts resorb |
| Wolff's Law | 'bones in a healthy animal will adapt to the loads placed upon them;' repeated actions will cause remodeling to become stronger while decreased loads will cause atrophy |
| Pseudo-pathology | Changes to bones that may appear as pathology but actually are the result of physio-chemical taphonomic processes |
| Health vs Disease | Can holistically be described as a continuum--"health is a state of complete physical, mental and social well-being and not merely the absence of disease or infirmity.” |
| Aetiology | The study of the cause of a disease |
| Idiopathic | A condition with unknown etiology |
| The medical tripod | Diagnosis, prognosis, treatment |
| How are conditions diagnosed in paleopathology | Macroscopic investigation, radiology, immunology (Ab), DNA, histology |
| Pathognomonic | A sign/symptom that is specifically characteristic of a particular disease |
| Equifinality | There are many potential methods to reach the same conclusion |
| Burden of proof | Equifinality requires researchers to rule out alternative explanations/acknowledge multiple interpretations |
| Underdetermination | The evidence available may be enough to eliminate some possibilities but not precisely narrow down the exact occurance |
| Three key concerns of the Osteological Paradox | Demographic non-stationarity (people move around), selective mortality (we are only sampling the deceased), hidden heterogeneity (individuals are not equally likely to contract a disease or suffer greatly from it; variable frailty or relative risk) |
| Explain the phrase "better health makes for worse skeletons" | The more resilient someone is in life, the more likely they are to survive disease and trauma, and have the marks of it on their skeleton--if someone contracts TB and dies immediately, they would not show the skeletal markers associated with the disease |
| Explain the phrase ‘A dog can have fleas and ticks too’ | Competing causes of death; just because a skeleton has lesions indicating one disease, doesn't mean they had to have actually died from it |
| Epidemiology | The study of disease and what causes it |
| Paleodemography | The study of the structure of past populations in a statistical manner |
| Arthritis | umbrella term referring to conditions involving the inflammation or degeneration of joints (over 100 disorders) |
| Arthrosis/Osteoarthritis (OA) | occurs due to repeated activity (also related to age, genes, lifestyle) in a joint, causing degeneration of the joint cartilage. may result in eburnation, sclerosis, osteophytes. most common joint disease |
| Eburnation | Creation of shiny, even scraped, surface due to bone on bone contact in affected joints |
| Subchondral sclerosis | Thickening (ie increased density) of the bone below the cartilage surface in affected joints |
| Osteophytes | 'bone spurs'; outward projections that form along the edges of synovial joints in response to articular cartilage damage and joint degen |
| Enthesophytes | Bony projections that form at the attachment points in the same direction of attachment (tendons, ligaments, joint capsules). result of chronic stress/inflammation or injury |
| Primary vs secondary OA | 1: age related deterioration, may be influenced by repeated activity 2: develops earlier in life directly related to trauma or bloo/bone disorder (Legge-Perthes) |
| Concomitant | Naturally accompanying: secondary OA is concomitant to trauma, osteophytes are concomitant to articular cartilage degen |
| Hypertrophic bone | hypertrophy: increase in cell size; bone tissue that has been enlarged |
| Hypertrophic OA | OA involving the formation of a considerable amount of osteophyte (marginal; larger joints ie acetabulum) |
| Atrophic OA | OA with minimal change/growth, occurs in small joints |
| Paucarticular | Occurs in a few joints ie with paucity |
| Schmorl's nodes | Asymptomatic depression in either inferior or superior surface of the vertebrae (the centre of the vert. bodies) |
| Rheumatoid arthritis (RA) | Multifactorial etiology, often in hands and feet; synovial membrane becomes inflamed -> swells and forms a pannus -> pain and destruction: subluxation, ankylosis, degeneration. Related to rheumatoid factor (RF) |
| Subluxation | The partial dislocation of a joint as in RA; facets still in contact but are not in normal alignment |
| Ankylosis | Fusion of bones at the joint resulting in immobility |
| Progressive RA | Most common, progressively gets worse |
| Intermittent RA | Experience periods of remission/inactive disease |
| Malignant RA | Least common, expresses painful (fatal) extra-articular symptoms |
| RF | The antibody produced in RA that autoattacks and causes disease; differentiates RA from seronegative (ie Ab-lacking) arthropathies |
| Four major seronegative arthropathies and what they have in common | Ankylosing spondylitis (AS), psoriatic arthropathy, reactive arthropathy (ReA, formerly known as Reiter’s syndrome), enteropathic arthropathy; no RF, always affects sacroiliac joint, results in spinal fusion |
| Ankylosing spondylitis | inflammatory condition often affecting entheses, affecting men more; very common and most easy to diagnose due to severe, continuous, symmetrical fusion of axial skeleton and erosion of vertebral bodies (Schmorl's), proliferation and no skip lesions |
| Psoriatic arthropathy (PsA) | Develops in some patients who have psoriasis, most commonly results in asymmetrical oligoarthritis: inflammation of SIJ, paravertebral bridging/spinal fusion with skip lesions, erosion of DIPs-> pencil in cup sign. Hard to diagnose osteologically |
| Reactive arthropathy | arthritis associated with infectious disease; results in asymmetrical fusion of one of both SIJs, spinal fusion (with paravertebral bridging and skip lesions), asymmetrical erosions of small joints (and possibly enthesophytes) in lower extremities. |
| Enteropathic arthropathy | occurs due to an association with gastrointestinal issues (ie IBS); usually monoarticular (often in knees) and symmetrical, no skip lesions, may have proliferation |
| Kyphosis | Outward rounding of the spine |
| Lordosis | Inward rounding of the spine |
| Scoliosis | Lateral rounding of the spine |
| Paravertebral bridging | The formation of bone bridges between vertebrae, often refers to the discontinuous condition involving skip lesions |
| Skip lesions | Patchy lesions that 'skip' over areas; when talking about spinal fusion, referring to how many conditions result in discontinuous fusion across multiple vertebrae |
| Arthritis mutilans | Type of PsA; the most destructive/disabling kind, also the most likely to be properly diagnosed in paleopathological contexts--results in severe changes in the phalanges, including shortening(resorption) distally and 'cup and pencil' sign; may resemble RA |
| Gout | Joint inflammation caused by precipitation of uric acid in/around joints; primary caused by purine metabolism defect, secondary by other conditions or by taking medication; skeletally, most recognizable when MTPJ involved |
| Risk factors for gout | overweight, overconsumption of alcohol, often eat rich/fatty foods high in purines (red meats) |
| Acute gout | sudden and intense pain, redness, swelling, often in first MTPJ; may go away or advance to chronic |
| Chronic gout | Characterized by 'gouty tophi:' swelling of soft tissue, composed of urate crystals--eventually results in asymmetrical polyarthropathy, almost always affecting first MTPJ |
| Spondylolysis | stress fracture through the pars interarticularis in the lumbar region (L5), activity-driven and a consequence of bipedal locomotion |
| Spina Bifida | Neural tube defect; an deformation in one or more vertebrae (posterior and medial) that may allow the spinal cord to escape a little or at least is a bit exposed; closed=asympt, open=hernia sac containing spinal fluid and meninges, may even neural tissue |
| Cleft neural arch | a break in the neural arch, a result of incomplete ossification; in the sacrum, far more severe and extends down even S1 thru S5 (and the arches look INCOMPLETE) |
| Klippel-Feil | used to describe the congenital disorder of cervical vertebrae fusion of both the bodies and posterior elements (in two or more vertebrae); results in block vertebrae (multiple, non-adjacent segments most common) and ventral hypoplasia |
| Anemia | when experienced in early life, causing overproduction of RBC-> shows as expansion of the diploe in cranial bones, porotic hyperostosis, cribra orbitalia |
| Vitamin C deficiency (Scurvy) | a historical disease & condition of class; vitC -> collagen synth. -> deformation of bones/increased resorption, thinning cortex, 'scurvy line', enlarged epiphyses in juveniles (looks almost like rickets), osteoporosis in adults |
| Vitamin D deficiency (Rickets/osteomalacia) | rickets in juveniles, OM in adults. caused either by lack of vitD, Ca, or mutation causing impaired PO4 use. rickets: fraying, porous epi/metaphyses; bowing, in walking children; rachitic rosary. OM: pseudo-fractures |
| Subperiosteal new bone (PNB) | deposition of new bone underneath an infected/inflamed periosteum (appears first as woven, active phase, THEN lamellar) |
| Osteomyelitis | umbrella term to encompass any inflammatory infection that affects bone or marrow. often affect the long bone metaphyses (slow blood flow and high porosity lets infection spread easier). may form cloacae due to increased pressure in medullary cavity |
| Tuberculosis | chronic infection caused by Mycobacterium tuberculosis (infective respiratory transmission) & bovis (from dairy, less common); primary infection may heal or progress to bloodstream & skeleton, prefer sponge & spine ->kyphosis from vert.body collapse |
| Leprosy | Tuberculoid: less severe, less likely to reach bones; Lepromatous: more severe, many lesions, nerve damage & involvement of the skeleton-- destruction of rhinomaxillary region (LOD) and extremities (concentric loss, most often feet/ankles) |
| Treponemal disease | Caused by Treponema pallidum and its subspp; includes Pinta, Bejel, Yaws, and venereal syphilis--only severe cases that have progressed to tertiary phase is the skeleton impacted (10-12% cases) |
| Venereal syphilis | incubation period -> primary phase: skin lesion 'chancre,' involvement of lymph nodes -> secondary: migration thru bloodstream, spread of rash/lesions -> tertiary: invasion of other organs, incl. skeleton. may involve gummatous necrosis. |
| Congenital syphilis | early (until 2yrs): widespread PNB and disruption of chondral ossification, most noticeable in fastest growing metaphyses (around the knee). symmetrical. later (after 2yrs): saber shin/pseudo-bowing, saddle nose, Hutchinson/mulberry teeth |
| Spina bifida skeletal signs | obvious in the sacrum, opening at the S1-S2 areas--note that opening/closing of the S4-S5 is a normal difference in phenotype |
| LOD | Leprogenic odontodysplasia: concentrically stunted roots (upper incisors) due to lepromatous infection during tooth development |
| Skeletal markers of syphilis | PNB formation and lesions of the bones closest to the surface to of the skin: tibia, face (cranium--frontal bone--and nasal cavity: caries sicca), ribs/sternum |
Created by:
camiebio
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