Nutritional Management On Musculosceletal Disease

Departemen Ilmu Gizi
FK-Unhas
September 2016
Nutrition in Musculosceletal systems 2016 1 02/09/2018
Based on SKDI 2012,
Level competence : 3A
* osteoporosis
* osteoarthritis
Level competence : 1
• Ricketsia
• Osteomalacia
Level competence :4A
 Hyperuricemia, gout
*
*Nutrient related to musculosceletal system
*Osteoporosis
*Osteoarthritis
*Ricketsia
*Osteomalacia
*Hyperuricemia, gout
*
*To understand nutrition related to musculosceletal
system
*To understand nutrition risk factor and nutritional
management related to osteoartritis
*To understand nutrient and nutritional management
related to osteoporosis
*To understand nutrient and nutritional management
related to gout, hyperuricemia
*
*

* The human sceletal systems consists of bones,
cartilage, ligaments and tendons.
* Bones are living, growing and changing parts of
the body.
* There are 3 bone cells :
* osteoblasts : the bone-forming cells
* osteoclasts : resorb or break down bone
* osteocytes : mature bone cells

* Bone strength is derived from quantity (density
and size) and quality (structure, consistency
and turnover).
* Bone mass is dependent on individual genetic
background.
* Adequate nutrient intake is needed from birth
to achieve maximal bone mass and to prevent
osteoporosis in later life.

* Sufficient protein intake
* Adequate calcium intake
This are supports stronger
bone density
• Omega-3 fatty acids such
as EPA (eicosapentaenoic
acid) helps increase
levels of calcium in the
body, deposit calcium in
the bones, and improve
bone strength.
*
* Vitamin D3 plays
important role In calcium
metabolism.
* Vitamin C and K are
cofactors of key enzymes
for skeletal metabolism.
* Sufficientfolic acid and
vitamins B6 and B12 can
help improve bone health.
* Antioxidant nutrients,
including provitamin A
and vitamin C also play a
role in bone health.
*
* The trace elements, calcium and phosphorus, are
highly involved in skeletal growth.
* Paratyhroidhormone (PTH) regulates calcium and
bone homeostatis.
* Magnesium and flouride are matrix constituents.
* Zinc, copper and manganese are components of
enzymatic systems in matrix turnover.
* Selenium as an antioxidant.
* Iron promotes production of collagen in bone
structure.
*
Table 1. Some important minerals in the bone
Element Total bone content (g) % Bone weight

Calcium 1000 25
Phosphate 400 10
Sodium 200 5
Magnesium 80 2
Zinc 8 0.2
Potassium 4 0.1
Strontium 0.8 0.02
Boron 1.6 0.04
Aluminium 0.8 0.02
Lead 0.4 0.01
Copper 0.08 0.002
*Bone is metabolically active tissue.
*In the adult, skeleton most metabolically active occurs by the
process of bone “remodelling” or bone turnover.
*This metabolically activity serves to maintain the structure and
homeostatic functions of the skeleton.
*Remodelling involves a defined sequence events. The process
of bone formation occurs at sites at which bone resorption has
recently occured.
*This integration between bone formation and bone resorption is
termed ‘coupling’.
*
Pre- Pre- 6H, PTH, IL-1
osteoclast osteoblast IL-6, -E2, T3
IL-6
Growth factors
IL-6 Osteoblast Binding protein
Osteoclast
60µm H+ Proteases
Binding Growth Binding Growth

protein factors protein factors
30µm
Resorption Formation
20 days 160 days
Figure 1. Normal bone remodelling
Rosen C. In: Marcus R, et al. Ed. Osteoperosis, Atlas of Clinical
Endocrinology, volume 3. Blackwell Science Publisher 2000.
*

* Rickets derived from the old English word for
"twist," or "wrick,“
* Rickets is caused by a deficiency in vitamin D.
* During growth, human bone is made and maintained
by the interaction of calcium, phosphorus, and
vitamin D.
* Calcium is deposited in immature bone (osteoid) in
a process called calcification, which transforms
immature bone into its mature and familiar form.
* In order to absorb and use the calcium available in
food, the body needs vitamin D.
* In rickets, the lack of this important vitamin leads
to low calcium, poor calcification, and deformed
bones.
*
Figure 2. Form of rickets in children
* Known as adult rickets, causes softening and
demineralization of the bone from insufficient vitamin
D.
* It may occur in conjunction with bone loss and hip
fracture.
* It more commonly results from intestinal malabsorption
as from Chron’s disease, colon resection, cystic fibrosis,
celiac disease or chronic use of anti-convulsants.
* The majority of patient have bone plain and muscle
weakness.
*
*
*Osteoarthritis is a disease characterized by
structural abnormalities at the joint level, a
common health problem in populations over age
40 years.
*It is a leading cause of pain and disability.
*The wrists, hips and spine are mostly affected.
*Osteoarthritis is the most common type of
arthritis.
*
* Obesity is an independent risk factor for
osteoarthritis.
* Biomechanical loading and metabolic
inflammation associated with excess adipose
tissue and lipids may have a role.
* Pain associated with osteoarthritis leads to
increasingly less activity and psychosocial and
physical disability.
* Physical inactivity is an independent risk
factor for inflammation due to the reduced
expression of systemic and cellular anti-
inflammatory mediators.
*
Figure 3. Relationship among osteoarthritis, obesity, physical
inactivity and chronic low-grade systemic inflamation
Figure 4. Healthy knee joint and osteoarthritis
22 02/09/2018
Nutrition in Musculosceletal systems 2016
* Maintain a normal body weight. If needed,
weight loss may be beneficial to lessen
pressure on weight-bearing joints. Use a
calorie-controlled diet if obesity present.
* Evaluate for sarcopenic obesity, which is
common with knee OA.
* Vitamin D and K play a protective role.
Encourage patient (especially if older) to
consume adequate amounts of vitamin D, and
K, protein and calcium from a healthy,
nutrient-dense, antioxidant-rich diet.
*
* Maintain integrity of cartilage in affected
joints. Omega-3 fatty acids may reduce the
activity of enzymes that destroy cartilage.
Diets rich in omega-3 fatty acids may reduce
joint stiffness and pain, increase grip strengeth
and enhance walking pace.
* Prevent falls. The risk of falling doubles in
those with lower extremities osteoarthritis.
* Maintain active lifestyle as much as possible.
*
* Nutraceutical research :
* the most effective : glucosamine, chondroitin, collagen
hydrolysates (CHs), and avocado-soybean unsaponifiables
(ASUs). Piascledine 300 mg (ASU) given once daily is as
effective as chondroitin sulfate 400 mg three times daily.
* Spices and herbs research :
* Curcumin is the yellow pigment isolated from the
rhizomes of Curcuma longa (turmeric). Arantal is a highly
bioavailable curcumin that has shown efficacy.
* An herbal-leucine mixture (HLM) containing extract of
Uncaria tomentosa, Boswellia spp, Lepidium meyenii and
L-leucine has also been found to be an effective anti-
inflamatory agent for OA.
*
*
* Osteoporosis is the most common
bone disease in humans.
* It is characterized by low bone
mass, structural deterioration and
decreased bone strength.
* The aging population is highly
affected.
* It is silent disease until a fragility
fracture occurs at the hip or
proximal humerus, when significant
physical disability can result.
*
Age-related bone development
in men and women
I Men
1,500
I III
Bone mass (g/calcium)
Women
1,000
II
III
500
I Peak bone mass
II Rapid bone loss (menopause)
III Age-related bone loss
0
0 20 40 60 80 100
Age (years)
Figure 5. Age-related bone development in men and women

*From middle-age onward, Bone Mineral Density
(BMD) decreases and bone quality deteriorates
with advancing age, resulting in loss of bone
strength.
*Especially in women, BMD decreases sharply in the
perimenopausal period and for several years
thereafter.
*In addition to this natural course, genetic factors,
nutritional deficiency since childhood and puberty,
lack of exercise, and unhealthy lifestyle also cause
loss of bone strength.
*

*Bone remodeling consists of bone resorption by
osteoclasts and bone formation by osteoblasts, a
mechanism to maintain bone strength.
*If bone resorption increases with advancing age
and menopause and exceeds the rate of bone
formation, BMD will begin to decrease.

Figure 6. Factors causing deterioration of bone strength

It cannot be altered
* advanced age
* caucasians (e.g Northern European and Asian)
* Female genders
* Family history of osteoporosis
* History of fracture in a first-degree relative
* Low body mass index and low muscle mass
* personal history of fracture after age 50 years
*
It can be altered
* anorexia nervosa
* current smoking
* depression, past or current
* diabetes
* estrogen deficiency (premature menopause, amenorrhea)
* excessive use of alcohols
* homocysteine, elevated plasma levels
* hypertension
* hypogonadism
* lifetime diet low in calcium (poor diet, excess fiber)
* low testoterone levels in men
* low vitamin D intake or UVB sunshine exposure
* sedentary lifestyle or extended bed rest (immobilization)
* use of chemotherapy, tamoxifen, glucocorticoids, lithium and some
anticonvulsants
* total parenteral nutrition, long-term use
*
Conditions or diseases that may lead to osteoporosis
* AIDS-HIV
Amyloids
* Ankylosing spondylitis
* Celiac disease
* Chronic obstructive pulmonary disease
* Congenital porphyria
* Cushing syndrome
* Diabetes type 1
* Gastrectomy
* Gaucher disease
* Hemochromatosis
* Hemophilia
* etc
*
Figure 7. Clinical presentation and prognosis of osteoporosis

DIAGNOSIS
BONE IMAGING
At present the mostly used bone imaging are :
Quantitative ultrasound (QUS)

Dual energy X-ray absorbtiometry (DEXA)
No single technology is likely to be ideal, particularly with respect to cost an
availability (Johnston CC, Amer J Med 1995)
DEXA is now the gold standard for the diagnosis

of osteoporosis
DIAGNOSIS
BONE IMAGING
Normal Osteoporosis
Normal Osteoporotic
Figure 8. Scanning electron microscopy of normal and osteoporotic bone
Dempster DW, et al. J Bone Miner Res 1986;1:15–21

http://www.helenhayeshospital.org/rbcmain.html
CLASSIFICATION OF
BONE MINERAL DENSITY LEVELS
DESCRIPTIONS MEANING
Normal BMD BMD above – 1 SD from the

young normal mean
Low BMD or osteopenia BMD between - 1 SD and –

2.5 SD
Osteoporosis BMD is reduced < – 2.5 SD
Severe or established BMD is reduced < – 2.5 SD in

osteoporosis the presence of fractures
WHO Technical Report Series. Geneva: WHO, 1994

3250
Projected to
Projected number of osteoporotic reach 3.250
million in
hip fractures worldwide Asia by 2050
668
742
400
378
600
629
1950 2050
Total number of
1950 2050
hip fractures:
1950 = 1.66 million
1950 2050
2050 = 6.26 million
100
1950 2050
Estimated no of hip fractures: (1000s)
Adapted from Cooper C et al, Osteoporosis Int, 1992;2:285-289

Treatment guidelines
Description Meaning Treatment

Normal BMD BMD above > - 1 SD from No
the young normal mean
Low BMD or
osteopenia BMD - 1 SD and – 2.5 SD Prevention
Osteoporosis BMD is reduced < – 2.5 SD Treatment
Severe or established BMD is reduced < – 2.5 SD Treatment

osteoporosis in the presence of fractures
* Advise all patients to consume adequate
amount of dietary calcium and vitamin D.
* If fluid milk is not consumed, dry skim milk
powder can be added to many foods. In most
cases, individuals with lactose intolerance do
not need to eliminate dairy consumption
completely.
* Calcium supplements should be used only if
dairy products are not tolerated, calcium
absorption averages approximately 30% to 40%
from most sources.
*
* Excess of calcium supplements can cause
hypercalcemia, monitor intakes carefully and
take no more than 500-600 mg (two or more
times daily with meals).
* Avoid taking with iron supplementation.
* Rates of calcium absorption vary and dietary
sources are the best absorbed. Calcium
maleate is also well absorbed.
* Side effects of calcium supplementation may
include abdominal pain, anorexia,
constipation, vomiting, nausea, or dry mouth.
*
* Space the supplement throughout the day with
meals. Use with vitamin D and magnesium.
* For vitamin D, choose fortified milk, cod liver,
egg yolks and fatty fish. Supplements may be
needed. Do not exceed 10.000 IU/d.
* Extra protein may be needed.
* For sufficient intake of vitamin B12, include
dairy products, meat, poultry, fish and fortified
cereals.
* Isoflavones may be also beneficial, use two to
three servings of soy food daily.
*
* If patient is obese, use a nutrient-rich,
calorie-controlled diet that provides adequate
protein, vitamins, calcium and others minerals.
* Adequate manganese, vitamins C and K,
potassium and magnesium should be
consumed to meet at least the DRI levels.
Include fruits and vegetables that contribute to
bone health.
* Assure that folic acid and vitamin B6 and B12
are adequate, especially if serum
homocysteine levels are elevated.
*
* Sodium must be controlled. Keep sodium within desired
limits while increasing potassium and magnesium.
* Beware of excess of wheat bran because phytates may
increase calcium excretion.
* Caffeine from coffee does not seem to be a problem if
calcium (as from milk) is consumed in adequate
amounts.
* Change a sedentary lifestyle. Aerobic and
strengthening exercise will be helpful.
* Decrease the use of tobacco.
* Encourage adequate exposure to sunlight (10 to 30
min/day). Avoid sunburn and overexposure, with its risks
of skin cancer.
*
*
* Gout is a metabolic disorder of
excess uric acid accumulation that
manifests as inflammatory arthritis,
chronic arthropathy, and the
formation of tophi, deposits of
monosodium urate crystals in the
joints and tendons.
* Uric acid is the end product of
purine metabolism.
* Human lost hepatic uricase activity,
this leads to uniquely high serum
uric acid concentrations when
compared with other mammals.
*
* Acute attacks may be triggered by surgery, sudden and
severe illness, fasting, chemotherapy, or joint injury.
* Gout progress from asymptomatic hyperuricemia to acute
gouty arthritis, gout with intervals between acute attacks,
and finally chronic tophaceus gout. Permanent tophi may
develop if the condition goes undertreated.
* Although attacks of gout can subside in a few days,
repeated attacks can cause permanent joint damage, and
the disease often results in substantial disability and
frequent medical care.
*
Figure 9. Synthesis and excretion of uric acid
Increased urate production Decreased renal excretion of
urate
• nutritional/food : excess • drug : ethanol, cyclosporine,
ethanol or fructose intake, thiazides, furosemide,
meat, seafood ethambutol, pyrazinamide,
• hematological : aspirin
myeloproliferative and • renal : hypertension, polycystic
lymphoproliferative disorders, kidney disease, chronic renal
polycythemia failure
• metabolic/endocrine :
• drugs :ethanol, cytotoxic dehydration, lactic acidosis,
drugs, vitamin B12 (treatment ketosis, hypothyroidism,
of pernicious anemia) hyperparathyroidism
• others : obesity, psoriasis, • others : obesity, sarcoidosis,
hypertriglyceridemia leukimia, toxemia of pregnancy
*
Figure 9. The pathogenesis of hyperuricaemia and gout.
Figure 10. Fructose and uric acid
Source : Pillinger MH et al. Hosp Jt Dis. 2008;66(3):231-9.
Figure 11. Inflamation stimulate hyperuricemia
Source : Anker SD et al. Circulation 2003;107:1991-7
*A low-fat, high-carbohydrate diet increases excretion of
urates.
* Reduces intakes of beef, organ meats, seafood, pork, bacon
and ham, use more soy-based or meatless meals.
* Nonfat milk, low fat yogurt, dairy products, fruits such as
cherries, and high intakes of vegetable protein may reduce
serum urate.
* Ensure a high-fluid intake, especially water, skim milk and
coffee.
* Exclude alcoholic beverages, fructose or sugar-sweetened
soft drinks.
* Use antioxidant-rich foods such as pomegranate,
raspberries and strawberries.
*
KANDUNGAN PURIN DALAM MAKANAN :
Golongan A ( 150 - 1000 mg purin/ 100g )

•Hati, ginjal, otak, jantung, paru, lain-lain jerohan, udang, remis,
kerang, sardin, herring, ekstrak daging, ragi (tape), alkohol,
makanan dalam kaleng.
Golongan B ( 50 - 100 mg purin/ 100g )

•Ikan yang tidak termasuk golongan A, daging sapi, kacang-
kacangan kering, kembang kol, bayam, asparagus, buncis, jamur,
daun singkong, daun pepaya, kangkung.
Golongan C ( < 50mg purin/ 100g )

•Keju, susu, telur, sayuran lain, buah-buahan.
*
*

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Departemen Ilmu Gizi

Nutrition in Musculosceletal systems 2016 5 02/09/2018

Nutrition in Musculosceletal systems 2016 6 02/09/2018

Nutrition in Musculosceletal systems 2016 7 02/09/2018

Element Total bone content (g) % Bone weight

Binding Growth Binding Growth

Nutrition in Musculosceletal systems 2016 14 02/09/2018

Figure 5. Age-related bone development in men and women

Nutrition in Musculosceletal systems 2016 29 02/09/2018

Nutrition in Musculosceletal systems 2016 30 02/09/2018

Nutrition in Musculosceletal systems 2016 31 02/09/2018

Nutrition in Musculosceletal systems 2016 35 02/09/2018

At present the mostly used bone imaging are :

Quantitative ultrasound (QUS)

DEXA is now the gold standard for the diagnosis

Figure 8. Scanning electron microscopy of normal and osteoporotic bone

Dempster DW, et al. J Bone Miner Res 1986;1:15–21

Normal BMD BMD above – 1 SD from the

Low BMD or osteopenia BMD between - 1 SD and –

Severe or established BMD is reduced < – 2.5 SD in

WHO Technical Report Series. Geneva: WHO, 1994

Estimated no of hip fractures: (1000s)

Adapted from Cooper C et al, Osteoporosis Int, 1992;2:285-289

Description Meaning Treatment

Osteoporosis BMD is reduced < – 2.5 SD Treatment

Severe or established BMD is reduced < – 2.5 SD Treatment

Golongan A ( 150 - 1000 mg purin/ 100g )

Golongan B ( 50 - 100 mg purin/ 100g )

Golongan C ( < 50mg purin/ 100g )

Nutrition in Musculosceletal systems 2016 57 02/09/2018

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