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ANTH 213 > anth 213 module 3 > Flashcards

anth 213 module 3 Flashcards

1
Q

paleostomatology

A

mouth and teeth disease of past pop, reconstructing dental and oral health and diet

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2
Q

whats the advantage abt paleostomatology?

A

aint no pseudo pathology and markers r super specific

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3
Q
A
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4
Q

this thing comes from alveolar resorption caused by diet issues, deficiencies, periodontal disease, cavities, tooth removal, bruxism

A

ante mortem tooth loss

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5
Q

“alveolar bone is repeatedly resorbed by osteoclasts and renewed by osteogenic cells. This means that an old bone is constantly being resorbed and replaced by a new bone.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044990/#:~:text=Periodontal%20diseases%2C%20also%20known%20as,replaced%20by%20a%20new%20bone.

A

alveolar resorption

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6
Q

from local demineralization caused by acid, bacteria, genetics, too much sugar, which is easy to identify and no taphonomies exist for this

A

dental cavity/caries

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7
Q

when minerals r removed from hard tissue, like teeth and shit

A

demineralization

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8
Q

describe the global trend of cavities/caries throughout the paleolithic, neolithic, and XVIth century periods

A

very few paleolithic, more in neolithic bc of more cereal and diet changes, even more since xvith century bc colonialism sugar and diet changes

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9
Q

pocket of pus in or near tooth bc of cavities/bacteria and can probs kill you

A

abscess

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10
Q

inflammation without infection around tooth roots bc of bruxism, intense chewing or dental wear

A

dental cyst

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11
Q

no dental cavity and no pus evac for the paleopathology ver of this disease

A

cyst

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12
Q

less enamel, proof of abrasive meal or bruxism, there was more b4 industrial revolution bc we eat chiller foods now

A

dental wear

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13
Q

involuntary tooth grinding

A

bruxism

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14
Q

inflamed periodontal area, gum loss, alveolar resorption but no tooth loss, caused by hygiene probs, bruxism, metabolic disease

A

periodontopathy

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15
Q

proof of a protein and meat lover, can analyze to find chem ele of fibers, ceral, pollen, other food

A

calculus/tartar

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16
Q

cementum develops around tooth root bc of biomech stress or inflammation, more common for neanderthals

A

hypercementosis

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17
Q

less enamel mineralization during tooth growth, proof of stress during early childhood but not specific

A

enamel hypoplasia

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18
Q

first molar/first incisor enamel dev issues, unknown cause, local dyschromia

A

dental hypomineralization

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19
Q

change in colour

A

local dyschromia

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20
Q

enamel base lesion without cavity/caries/infection caused by biomech impact, more common back in the day bc our food is chiller now

A

dental mylolysis

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21
Q

what r some weird anomalies that happen during tooth development leadin gto dental malformation?

A

enamel pearl, teeth fusion

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22
Q

at least 1 tooth in palate/between normal teeth, retain baby teeth

A

supernumerary tooth

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23
Q

weird alveolar bone growth of mandible, prone for asians, caused by genetics and used to link family members together

A

mandibular torus

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24
Q

name all esthetic cultural teeth practices

A

filing, sharpening, incrustation

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25
Q

cultural teeth practice bc of specific use of mouth and teeth linked to diff jobs

A

functional

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26
Q

name 2 examples of med treatment for cultural practices on teeth

A

ligature w metal wire, metallic implant

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27
Q

how od we determine age of skeleton

A

tooth eruption, coffin size, how many adult-sized bones were in coffins w bones n teeth

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28
Q

who empirically have much larger teeth than others, and have to be excluded from determining age based on tooth size?

A

aussie aboriginals

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29
Q

what causes brown staining on teeth?

A

smoking/chewing tobacco

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30
Q

what should we not do when tryna analyze structural and cultural violence?

A

assume that no direct evi means there was no violence

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31
Q

what happened to bones of binded feet?

A

rotated or lost, not deformed

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32
Q

what was more common among women w binded feet?

A

more low femoral neck bone density, osteoporosis, healed fractures, hip fractures bc of falling from tiny feet instability

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33
Q

where do women w neck rings come from? (DOUBLE CHECK THIS W READING NOTES*)

A

padaung

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34
Q

where on the body was there direct evi for neck rings?

A

maxillomandibular facial dimensions

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35
Q

what r risks for neck rings, corsets and foot binding? (the second one is only for neck rings and foot binding btw)

A

immobilization and low bone density

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36
Q

what shape were the pelvi of women wearing corsets?

A

figure 8

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37
Q

chem rxn that preserve life via synthesis and degredation

A

metabolism

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38
Q

fucked up metabolism bc of genetics or acquired condition

A

metabolic disease

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39
Q

metabolism that leaves traces on bones

A

phospho-calci metabolism

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40
Q

what hormones control phospho calcic metabolism?

A

vit d, pth, calcitonin

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41
Q

hormone controling osteoblast activity

A

calcitonin

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42
Q

hormone controling osteoclast activity

A

parathyroid hormone

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43
Q

hormone controling mineralization and metabolic reg of calcium and phosphorus

A

vit d

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44
Q

these 2 disesases r caused by vit d deficiency bc of diet or genes

A

rickets in kids, osteomalacia in adults

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45
Q

semiology/symbols of rickets: default of mineralization of the bony matrix
▪ ______ of bone extremities due to mechanical loads
▪ ______________ of long bones
▪ ________ growth area
▪ Bone fragility and ____________
▪ Default of dental mineralization : _________
▪ Wide _______________________

A

rickets: widening, axial deformation, porous, pseudofracture, hypoplasia, dental pulp cavities

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46
Q

incomplete development of organs/tissues

A

hypoplasia

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47
Q

how do we usually identify rickets in osteoarchaeology

A

looking at residual bending deformity in long bones

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48
Q

deformation in osteomalacia is ______ bc it needs strong deformation during growth

A

rare

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49
Q

osteomalacia has the same sings as osteoporosis but w ___________ too

A

pseudofracture

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50
Q

osteomalacia diagnosis is not the same as vicious callus type ok if you agree

A

ok

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51
Q

vascular disease caused by no vit c and fragile blood vessels

A

scurvy

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52
Q

semiology of this disease:
- bleeding and _________
- ___________
- new ________ formation
- high _________ and _______ _____________
- deformation of _____ _______ extremities and radiographic “_______ ______”
- ______ loss and __________ ______________

A

scurvy: osteopenia,inflammation, bone, porosity,cribra orbitalia, long bone, scurvy lines, tooth, alveolar resorption

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53
Q

which two diseases can coexist during childhood?

A

rickets and scurvy

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54
Q

what disease has less bony matrix mineralization

A

rickets

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55
Q

what disease has less bony matrix formation aka ob activity and as a result has shit skel conservation bc of the porosity and bc of that, it’s easier to analyze teeth instead bc theyre super super obvi

A

scurvy

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56
Q

semiology of this anemia:
- widening ________ _______ and narrower _______ ______
- porous ______ __________ and inflating _______ bone
- _______ __________, ________, tibiali

A

anemia: medullar cavity, compact bone, cranial hyperostosis, dipole, cribra orbitalia, femori

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57
Q

disease caused by folic acid deficiency during pregnancy

A

spina bifida

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58
Q

semiology of this disease:
- unfused ______ or _______ _________ on baby’s back
- partial or complete exit of ________ __________
- potential _______________ consequences

A

spina bifida: sacrum, lumbar vertebras, spinal column, neurological

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59
Q

disease w unknown, probably metabolic, cause

A

paget disease

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60
Q

semiology of this paget disease
- __________ and _________ pelvic and leg bones
- deformed bones bc of _____________ _______
- thicker _________ _______

A

paget disease: wider, weaker, mechanical load, cranial bone

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61
Q

what 5 things do u do to read a fracture?

A
  • date the fracture lifespan
  • indirect or direct mechanical identification
  • functional consequences
  • deduce what the treatment was for that disease
  • identify potential complications
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62
Q

when a fracture happened far from the death date:
- wound is fortified with _______ _______
- more or less _______ in function of fracture lifespan
- for adults, it takes ___ months to repair bone even tho there might still be some _________

A

osseous callus, porous, 3, calluses

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63
Q

when a fracture happened near the death date:
- theres no finished _________ or bone
- _____________ _______ at fracture site
- repairs process depends on _________ _______, ______ and ________________ origin
- _______ fracture ______

A

consolidation, accelerated growth, skeletal region, age, geographical, sharp edges

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64
Q

type of impact trauma near the fracture point

A

direct trauma

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65
Q

type of trauma where fracture forces r far from the actual site of fracture

A

indirect trauma

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66
Q

indirect trauma forces that are parallel to the bone going in opposite directions

A

tension

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67
Q

indirect trauma forces that r parallel to the bone converging in the same direction

A

compression

68
Q

indirect trauma forces that r twisting the bone in opposite directions

A

torsion

69
Q

indirect trauma forces that are literally tryna fold the two extremities of the bone (ouch)

A

flexion

70
Q

indirect trauma caused by forces perpendicular to the bone going in opposite directions

A

shearing

71
Q

direct trauma type caused by breaking horizontally bc of falling or a sharp object

A

transversal fracture

72
Q

theres a special case for transversal fractures for ______ fractures and _______ fracture

A

stress, rickets

73
Q

direct trauma type caused by star shaped scar/hole on skull that impacts the rest of skeleton too, many bone fragments

A

penetrating object fracture

74
Q

direct trauma type caused by heavy dull object compressing the bone, which leaves a mark on it but doesn’t go through the bone completely

A

crush fracture

75
Q

bones can try to absorb the impact of a force, doesn’t always work obvi which is why sometimes they fracture

A

bone elasticity

76
Q

indirect trauma type caused by flexion and rotation, risks shortening the bone and having hte bone pieces moving

A

oblique fracture

77
Q

indirect trauma type caused by torsion, risks bone fragments moving and shortening the bone

A

spiral fracture

78
Q

indirect trauma type caused by flexion, only possible on children bc their bones r immature

A

greenstick fracture

79
Q

indirect trauma type caused by compression, risk of complications like secondary arthrosis, osteophytosis, special case w vertebral settling

A

buckle

80
Q

indirect trauma type caused by compression in spongious bone, little risk of bone fragments moving or shortening

A

impaction

81
Q

indirect trauma type caused by a pulling force caused by strong muscle contraction, can remove the bone at the muscle insertion site

A

tearing off

82
Q

a possible complication in traumatology where the body creates new articulation, if the 2 pieces of a broken bone never heal, they’ll basically turn into 2 new and separate bones and the body creates a new articulation bc of that

A

pseudo-arthrosis

83
Q

bone shortening bc of their parts not aligning properly, can become kind of angled

A

vicious callus

84
Q

articulation/joints get deformed bc of biomechanical changes, joint wear

A

secondary arthrosis

85
Q

secondary infection due to an open fracture where the pressure against the bone caused by the pus and germs from the infection is too much, so it makes a hole in the bone and drains out from there. if the pus goes into the blood, the blood will carry that shit everywhere

A

osteomyelitis

86
Q

murder and execution r examples of this kind of violence

A

interpersonal violence

87
Q

war, raids, and genocide are examples of this violence

A

interpopulational violence

88
Q

drilling/making holes in the skull

A

trepanation

89
Q

list the 4 examples of interpersonal violence discussed in class

A

decapitation, sword stroke, arrow shot, bullet shot

90
Q

what r the 2 examples of surgery that were discussed in class

A

trepanation, amputation

91
Q

who mainly practiced cultural artificial cranial deformation

A

indigenous latin americans

92
Q

growth and maturation of an element, with a change
of form

A

development

93
Q

describe human growht timeline which btw is unique to primates

A
  • 0-4 years = fast development
  • 4-puberty =
    slower growth
  • puberty-adulthood = second fast development
94
Q

motor development is not advanced, long motherhood
dependence, undeveloped brain, short and multiple pregnancy

A

Altriciality

95
Q

ong and unique pregnancy, advanced sensitive and
motor development, developed brain, already partially autonomous

A

Precociality

96
Q

what does VITAMIN stand for

A

Vascular, biomechanical Impact, Trauma,
Anomalies, Metabolism, Infection, Neoplasic (abnormal cell/tissue growth)

97
Q

growth anomaly
- Deformity of some blood vessel
at the growth area of the bone
* Causing deformed limb

A

vascular growth anomaly

98
Q

growht anomaly where theres lots of physical impact or weight on biological tissues, Activity marker of child : Scheuermann disease
Alteration or destruction of linking cartilage of growth area due
to heavy loading on childish skeleton

A

biomechanical Impact

99
Q

growth anomaly, Alteration or destruction of linking cartilage of growth area due
to heavy loading on childish skeleton

A

Scheuermann disease

100
Q

growth anomaly - what r the 3 cases that create abnormal limb growth

A

▪ Destruction of growth cartilage
▪ Congenital pseudarthrosis
▪ Vicious callus
Growth anomalies

101
Q

pseudoarthrosis aka fracture that happens when “ a broken bone fails to heal after a fracture unless intervention (surgery) is performed. “ –topdoctors.co.uk but its there from birth , trauma growth anomaly

A

Congenital pseudarthrosis

102
Q

growth anomaly, genetical pathologies that influence
bone growth and development that r there since birth

A

congenital bone disease growth anomaly

103
Q

grwoth anomaly +/- 250 different symptoms that lead
to in proportion or disproportionate dwarfism

A

Osteochondrodysplasia

104
Q

abnormal stitch of bones in the skull, the spine or
the limb extremities areas, growth anomaly, cranial and post cranial

A

Dysostosis

105
Q

Osteochondrodysplasia, “Achondroplasia is a genetic condition affecting a protein in the body called the fibroblast growth factor receptor. In achondroplasia, this protein begins to function abnormally, slowing down the growth of bone in the cartilage of the growth plate.” johns hopkins medicine, growth anomaly

A

Achondroplasia

106
Q

growth anomaly, Imperfect osteogenesis
“Osteogenesis imperfecta (OI) is an inherited (genetic) bone disorder that is present at birth. It is also known as brittle bone disease. A child born with OI may have soft bones that break (fracture) easily, bones that are not formed normally, and other problems.” - johns hopkins medicine

A

Osteochondrodysplasia,

107
Q

osteochondrodysplasia but a lysosomal enzyme function weirdly “accumulation of harmful byproducts, namely, heparan sulfate, dermatan sulfate, and keratan sulfate” -wikipedia, growth anomaly

A

Enzymatic disorder

108
Q

premature fusion of skull bone parts, type of dysostosis and growth anomaly

A

crouzon’s diseas

109
Q

present at the birth or during the growth
and not systematically linked with a genetical disorder, growth anomaly

A

Developmental anomalies

110
Q

no upright setting during formation, affects foot, grwoth anomaly.

A

Clubfoot

111
Q

grwoth anomaly, hand or foot deviation

A

Fibular or radial aplasia

112
Q

grwoth anomaly, absence of limb

A

Phocomelia

113
Q

grwoth anomaly, more or less than 10 fingers

A

Abnormal dactyly

114
Q

grwoth anomaly affecting vertebral dev

A

Congenital scoliosis

115
Q

grwoth anomaly, bone fusion

A

congenital kyphosis

116
Q

“generalised disorder of skeletal growth and bone and cartilaginous tissue development
results in an abnormal shape of the limbs, trunk or skull. […] Direct palaeopathological findings of
these systemic defects in historical skeletal remains are very rare, as their incidence in the population
is lower than in other groups of diseases and differential diagnosis of these conditions is difficult” vargova et al 2023 what is this talking abt

A

bone dysplasia

117
Q

growth anomaly
Disorders due to a deficiencies or hormonals problem
▪ Deficiencies : rickets, scurvy, anemia, …
▪ Hormonals problem : in proportion dwarfism or gigantism,
acromegalia

A

Metabolism growth anomaly

118
Q

metabolic growth anomaly, body makes too much growht homrone/hGH during adulthood and abnormal proportions in the body all your life

A

acromegalia/acromegaly

119
Q

inflammation/infection growth anomaly:
inflmamed growing joint usually on knee → growth delay, osteoporosis, mechanival disorders
- willl create growth problems

A

juvenile arthritis

120
Q

“overgrowth disorders are those in which all or most of the parameters of growth and physical
development exceed 2 SD above average” - minozzi et al 2015 which dieseas is this talking bout

A

gigantism

121
Q

neoplasic growth anomaly, “a chronic disorder in which scar-like tissue grows in place of normal bone” - johns hopkins medicine

A

fibrous dysplasia

122
Q

pathological states present at given time in given pop, created in 1969 by M. grmek, historian of medicine

A

Pathocenosis

123
Q
  • porous bone linked w anemia bc of genes, infection or deficiency, no consensus on dev origin
    • cribra orbitalia
    • cribra humeri/femori
    • spongious hyperostosis
A

Porotic syndrome

124
Q

all living orgs coexist at biotope at the same place and time, which can change and adapt

A

Biocenosis

125
Q

stopping ameloblast creation, punctual lack during crown thickness dev → more reliable nonspecific stress marker

A

Linear enamel hypoplasia

126
Q

change in pathocenosis balance bc of socio/enviro/eco factors

A

Emergence/reemergence

127
Q

osteoarticular aging marker which means u have long and healthy life → osteological paradox

A

Degenerative joint disease

128
Q

environmental factors for disease

A

Pathoecology

129
Q

metabolic aging disorder where ligament and muscle insertion sites r calcified, unknown causes for males >45 y

A

Hyperostosis

130
Q

the enviro/haven that has a community of parasite/host/vector/pathogens living and circulating there→ made by en pavlovsky
one nidus = transmission/pathogens/niche/host easily predictable PROBS BC THEYRE ALL IN THE SAME PLACE

A

Nidus

131
Q
  • less bony mass, less lamellas and thinner compact bone, caused by less ob activity and vit d creation
    • more risks of fracture
A

Osteoporosis

132
Q

kids per women

A

Fertility

133
Q
  • population exposure to trauma
    • daily life
    • interpersonal and interpopulational violence
    • med/religious/cultural practices
    • be careful of taphonomy and paleopathomimic
A

Paleotraumatology

134
Q

osteological paradox mistakes worst skeleton = best health
state” - J. wood

A
  • mistake 1: unstable disease characteristics → we’ll never know how prevalent a disease is w/o stable demography which is impossible
  • mistake 2: mortality selectivity → some diseases r age selective → more death in 1 age group, therefore overestimation of prevalence compared to acc society → sample bias
  • mistake 3: variable sensitivity to disease → ppl respond diff to same disease → pops can be highly resistant, resistant, and weak → lesions only show up on resistant pop bc everyone else is dead (weak) or fully recovered (highly resistant)
135
Q

bone remodeling, cony lamella made w mineralized collagen round blood vessels

A

Osteon

136
Q

bone cell that buidl new bone/ossifies and is a stem cell

A

osteoblast

137
Q

bone cell that crubles/destroys old bone

A

osteoclast

138
Q

bone cell derived from osteoblast, stays in calcified matrix on inside of the boney matrix unlike ob and oc

A

osteocyte

139
Q

bone rebuilds after tiny microracks eps during disease

A

bone remodelling

140
Q

radiographic opaque line horizontal on bones which indicate growth restarting and formed during linking cartilage growth but later ossified. disappear after remodelling “lines of increased bone density that represent psotion of the growth plate” –first google sources

A

harris line

141
Q

What is the biocenosis concept?

A

Answer: All living organisms coexisting in a biotope.

142
Q

What does pathocenosis balance refer to?

A

Answer: Balanced ecology within a pathocenosis.

143
Q

Explain the concept of pathocenosis dynamic.

A

Answer: Changes in disease frequency and distribution over time.

144
Q

what r the diff disease interactions

A

Symbiosis/synergy: Degenerative + metabolic disease.
Antagonism: Plague rise = leprosis decline.
Indifference/independence: No effect on each other’s frequency.

145
Q

What are the difficulties in recognizing complete pathocenosis?

A

Answer: Diagnosis ambiguity, incomplete inventory, observation of only global tendencies.

146
Q

What are the principles of epidemiological transition?

A

Mortality - Population dynamics.
Transition - Shift from infectious to aging diseases.
Epidemiological transition - Changes in demographics and reproductive potential.
Important modifications - Demographic and socioeconomic changes.
Three models of transition - Classic, accelerated, delayed.

147
Q

Name the stages of epidemiological transition.

A

Pestilence and famine.
Decrease of pandemic period.
End of transition.

148
Q

What are the three conceptual mistakes of the osteological paradox?

A

Answer: Unstable disease characteristics, mortality selectivity, variable sensitivity to disease.

149
Q

List the functions of the skeleton.

A

Answer: Support, protection, hematopoiesis, mineral homeostasis.

150
Q

Describe endoconjunctive ossification.

A

Answer: Ossification from connective tissue on skull, face, clavicle.

151
Q

Explain endochondral ossification.

A

Answer: Conversion of cartilage into bone, excluding specific areas like the skull.

152
Q

What are the characteristics of woven bone?

A

Answer: Fragile, porous, in-progress.

153
Q

Define lamellar bone.

A

Answer: Dense outside, surround osteons, what woven bone is like after remodeling w osteocyte, oc and ob

154
Q

How does aged collagen influence bone quality?

A

Answer: Higher cross-link density, which makes it less elastic and more rigid, leading to easier fractures. happens w age too

155
Q

What are microcracks in bones?

A

Answer: Cracks that help toughen bones and signal remodeling.

156
Q

Name the lesional categories in histology.

A

Vascular, biomechanical impact, trauma, abnormality, metabolic, inflammatory, neoplastic.

157
Q

Give examples of specific markers of stress.

A

Answer: Rickets, scurvy, anemia, osteophytosis.

158
Q

What are some unspecific markers of stress?

A

Answer: Harris lines, porotic syndrome, linear enamel hypoplasia.

159
Q

What is the controversy with the study of Harris lines?

A

Answer: Uncertainty about whether they are pathologic or part of normal development.

160
Q

What are the advantages of studying aging diseases?

A

Answer: Frequently encountered, easily identifiable, age and sex-dependent.

161
Q

Name the different types of arthrosis.

A

Answer: Primary–idiopathic aka has no known cause, and secondary –articulation/joints get deformed bc of biomechanical changes, joint wear

162
Q

Explain the criteria of osteoporosis and osteopenia.

A

Answer: Osteoporosis involves decreased bone mass and changes in microarchitecture, while osteopenia is a natural decrease in bone mass.

163
Q

Describe hyperostosis.

A

Answer: Calcifying disease linked to metabolic disorders, characterized by new bone formation at ligament and muscle insertion sites.

164
Q

What are the types of trauma?

A

Answer: Direct and indirect.

165
Q

What are the steps involved in reading a fracture?

A

Answer: Dating, mechanical identification, functional consequences, treatment deduction, potential complication identification.

166
Q

How do ancient fractures differ from recent ones?

A

Answer: Ancient fractures show signs of repair but may not be fully consolidated, while recent fractures lack finished repair.

ANTH 213 (4 decks)

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