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Arthritis Flashcards

1
Q

what is bone made of

A

a calcified extracellular matrix (ECM)
made of inorganic ions

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2
Q

what are osteoblasts

A

make bone by secreting collagen and calcium salts

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3
Q

what is an osteocyte

A

derived from osteoblasts and sits in a small chamber called a lacuna
it maintains the bone

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4
Q

what are osteoprogenitor cells

A

stem cells in the bone that make new osteoblasts as osteoblasts cant divide into new ones

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5
Q

what are osteoclasts

A

bone resorption
they come from white blood cells
osteoclasts cause proteolytic enzymes and hydrochloric acid to resorb bone

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6
Q

what is bone homeostasis

A

this means that there is no net gain or loss of bone

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7
Q

what are the different types of bone that are laid down

A
  1. first woven bone/immature bone
  2. secondary bone is split into:
    -cortical/lamellar- dense, compact
    -cancellous- spongy- this is below the roots of teeth
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8
Q

how does vitamin D relate to bone formation

A

vitamin D increases calcium and phosphate
vitamin D comes from sunlight or diet e.g. fish
vit D increases the uptake of calcium in the small intestine

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9
Q

what are rickets

A

curved legs from vit D deficiency

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10
Q

what does the parathyroid gland do

A

secretes the parathyroid hormone(PTH) which increases calcium and phosphate in the blood by promoting the kidneys to make vit D and reabsorb calcium into the blood

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11
Q

what are the 2 types of thyroid gland malfunctions

A
  1. primary hyperparathyroidism
  2. secondary hyperparathyroidism
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12
Q

what is primary hyperparathyroidism

A

increased parathyroid hormone levels
often due to an adenoma (benign tumouor)

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13
Q

what does secondary hyperthyroidism do

A

-it causes calcium salts in CKD chronic kidney disease
- it compensates for this the parathyroid gland secretes more parathyroid hormone
- it increases bone resorption
- it leads to renal osteodystrophy (when the kidneys cant maintain calcium and phosphate levels )

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14
Q

how does hyperparathyroidism affect the jaws

A

very rare but can present as central giant cell granuloma
if a pt has this alongside hyperthyroidism it is termed- brown tumour of hyperparathyroidism

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15
Q

what are the stages of bone fractures

A
  1. the early infalmmatory stage
  2. the repair stage
  3. the remodelling stage
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16
Q

what does the early inflammatory phase of bone fractures consist of

A
  1. bleeding occurs at the fracture site and forms a hematoma (blood clot)
    - inflammatory cells and fibroblasts infiltrate the site - TNF (tumour necrosis factor) alpha, IL1,6,10,12, TGF (transforming growth factor)
    - blood vessels go into the hematoma and granulation tissue forms
    -
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17
Q

what does the repair stage of bone fractures consist of

A

-the granulation tissue formed in the inflammatory stage turns to callus
- primary callus turns to secondary callus by endochondral ossification
- osteoids are secreted into the area forming new bone
cartilage calcified due to BMPs, TGF-betas, IGFs, osteocalcin, collagen I, V and XI
- collagen forms in the area forming new bone

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18
Q

what does the remodelling stage of bone fractures consist of

A

redistribute compact and oven bone
orgnised osteoblastic and osteoclastic activity coordinates remodelling

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19
Q

what factors impact bone fracture healing

A

blood supply to the fracture
infections
if the fracture is closed or compound (pierces the skin)
the amount of bone or soft tissue loss
diabetes, radiotherapy, long term corticosteroids use (a steroid anti inflammatory e.g.eczema cream)
use of NSAIDS (IBUPROFEN, aspirin a non steroid anti inflammatory)
smoking
nutritional status
risk of future falls

20
Q

name the bone diseases we need to know about
name the arthritides we need to know about

A

bone diseases-
osteogenesis imperfecta
osteopetrosis
osteopenia and osteoporosis
pagets disease

arthritides-
osteoarthritis
rheumatoid arthritits
ankylosing spondilitis

21
Q

what is osteogenesis imperfecta

A
  • inherited condition where defects of collagen stop normal biomineralisaiton of the bone
  • caused by a type 1 collagen mutation
  • partial or complete absence of collagen
  • :. brittle bones
  • grey/blue discolouration of sclera
    oral features:
    skeletal class 3 pattern
    open bite
    impacted molars
    thin grey brown enamel
    delayed or premature eruption
    dentine can look opalescent - dentinogenesis imperfecta
22
Q

what is osteoPETrosis

A

a genetic condition where osteoclasts dont resorb bone
bone becomes harder and more marble like :. less flexible when stressed
- bone becomes more dense and opaque on radiographs
- more inorganic component of bone :. bone marrows hematopoietic ability (making blood vessels decrease)
delayed tooth eruption can lead to nerve entrapment :. low blood supply

23
Q

what is osteopenia and osteoporisis

A

osteopenia = bone has thinned
the degree of bone thinness using a DEXA scanner
osteopenia= -1 to -2.5
osteoporosis- lower than -2.5
can happen due to a bit D deficiency in youngsters
it Is normal to some degree in adults due to lack of bone protecting oestrogen after menopause and androgen in males

osteoporosis:
affects mainly vertebra, femur and wrists
can happen to people with COPD from coughing
kyphosis can occur - spine bends forward

24
Q

what factors increase bone loss

A

lifestyle- high caffeine, salt, low BMI (anorexia) , alcohol, smoking, immobility

genetic factors- females, family history of osteoporosis

endocrine- early menopause
hormonal changes
amenorrheoea- lack of periods

diseases-
cushings
hyperthyroidism
hyperparathyroidism

drugs -
Glucocorticoids (aka corticosteroids) Thyroxine
Heparin
Diuretics e.g. furosemide
Cytotoxic drugs

25
Q

what race are less likely to have bone loss

A

afro- caribbeans

26
Q

what drugs prevent bone loss

A

bisphophonates
HRT (hormone replacement therapy)

27
Q

how would you manage osteoporosis

A

pt lifestyle advise - vit D, low alc/smoking etc, low salt and caffeine

pain relief- AVOID NSAIDS, take para or physio

physio to stay mobile

physical aids- walking sticks

meds to prevent further bone loss-
vit D
bisphosphonates
SERMS (selective aoestrogen receptor modules
hormone replacement therapy
testosterone tx
regular med reviews with the GP
surgery to fix fractures

28
Q

what is pagets disease

A

increased resorption from overactive osteoclasts cause a response where osteoblasts become more active and secrete larger and weaker bone

can affect 1 bone or several
common in pelvis and spine
constant dull one pain
be careful when giving lengthy dental appointments
there can be cranial nerve deficits e.g. conductive deafness if the skulls foramina is in the path of this bone growth
pagets can lead to enlarged maxillae or mandible
hypercementosis- ossifying of the PDL

29
Q

what are some tx of pagets disease

A

bisphosphonates
analgesia
physiotherapy
surgery - if joint damage

30
Q

what are the 3 types of arthritides

A

osteoarthritis
rheumatoid arthritis
ankylosing spondilitis

31
Q

what is osteoarthritis

A

a wear and tear degeneration of the joints
low level chronic inflammation of the joints
effects the large weight bearing joints such as hips and knees but also some small like wrists

32
Q

what are features of primary osteoarthritis

A

synovial softening, tearing of articular cartilage, development of subchondral bone cysts and development of bony spurs or “osteophytes” in the joint itself

due to obesity or lack of physical exercise

33
Q

what are features of secondary osteoarthritis

A

develops following trauma of some sort, pain and stiffness in bones, fracture of the TMJ can lead to OA in the long term

34
Q

how can Osteoarthritis affect daily life

A

mobidity rate increases
limitations in functioning
impacts daily activity
impacts quality of life

35
Q

what symptoms does OA usually present with

A

stiffness after movement of a joint
e.g. painful knees after gardening
can be swelling of the joints but usually non inflammatory :. no redness or heat involved
with long term disease, the swelling can become bony rather than soft tissue resulting in herberdens nodes in dip joints of hands

36
Q

what is the managment of OA

A

pt management programmes
weight loss for obese pts
physio and walking aides
topical NSAIDS
Intra-articular corticosteroid injections for single, painful joints
Intramuscular corticosteroid injections for more widespread arthritis
surgery

37
Q

what surgical managements can be used to treat OA

A

1.Arthrocentesis or arthroscopies (direct endoscopic visualisation of the joint space +/- washing out of the joint, removal of osteophytes etc)

  1. Osteotomies (removal of bony deformities by surgical means)
  2. Arthrodesis (surgical fusion of a painful or unstable joint)
  3. Total joint replacements.
38
Q

what is rheumatoid arthritis

A

this is more suddenly occuring joint problem than OA. occurs more in younger people (under 40) compared to progressively occurring in older people for OA.
It is SYMMETRICAL. both right and left sides are affected
this is a multi system disease :. doesn’t only affect joints but also systemically e.g. neurological, renal,pulmonary (see other card)

39
Q

what are clinical signs of rheumatoid arthritis

A

“calor, dolor, rubor, tumor, functio laesa”) i.e. acombinationofheat,pain,redness,swellingandlossoffunction

early morning stiffness which takes hours to subside

40
Q

what are the systemic effects of rheumatoid arthritis

A

opthalmological- keratoconjunctivitis sica (dry eyes), sclera etc
hematological (sjogens)
pulmonary
gastrointestinal
dermatalogical
musculoskeletal

41
Q

what is ankylosing spondilitis

A

another chronic inflammatory arhtirits specifically affecting neck and spine
more prevalent in males
genetic predisposition- HLA-B27, HLA-B60, HLA-DR1

42
Q

how does ankylosing spondilitis present

A

this starts by sacroilitis -inflammation of the sacro iliac joints (where the pelvis meets the spine)
this then progresses up the vertebraes until it reaches the neck
this gives a slanting forward posture known as the question mark posture

43
Q

how would we manage ankylosing spondilitis in dental setting

A

pillow, shorter pts, adjust chair for neck support

44
Q

what is the difference between ankylosing spondilitis and OA and rheumatoid arthritis

A

mainly targets spine over distal or periphral joints (e.g. wrists)

45
Q

what commonly presents with autoimmune diseases such as OA and RA

A

these can go on to develop other Autoimmune diseases as they target other tissues e.g. inflammatory bowel disease and crohns

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