پروفسور محمد حسین سلطان زاده

استاد دانشگاه علوم پزشکی شهید بهشتی

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oWhat is Rickets?


o Rickets is the failure of osteoid to calcify in a growing child and this is most commonly caused by a lack of vitamin D .

o The adult equivalent is osteomalacia.


oWhy is Rickets reappearing ?


o  There has been an increase in exclusive BF for prolonged periods without vitamin D supplementation.

o  Human milk is low in vitamin D, & AAP recommends vitamin supplementation for breast-fed Infants.

o  Reduced maternal sunlight exposure reasons has become more common .


oWhat is the best   X-Ray view to obtain for evaluating possible rickets ?


o Anterior view of the knee, incorporating femoral & tibial metaphyses and epiphyses .

o Bone growth is most rapid in this area , and rachitic changes are seen earliest at this location.


oWhat X-Ray changes are noted in patients with rickets ?


o Cupping , Fraying, & Irregularity of the metaphyses .

o Widening of the physis as a result of increased osteoid.

o Loss or increased separation of the zone of provisional calcification .


oPeriosteal reaction

oCoarsening of trabeculae

oLoss of bone density

oBowing of long bones.


oWhat are the physical signs that were suggestive of rickets ?


o The anatomic abnormalities of rickets result primarily from the  inability to normally mineralize osteoid

o The bones become weak & subsequently distorted .

Signs of rickets include

o Craniotabes

o Femoral & Tibial bowing

o Delayed suture & fontanel closure

o Pigeon breast sternal protrusion as a result of use of accessory muscles

o Frontal thickening

o Detective tooth enamel

o Harrisons groove

o Palpably widened physes at wrists & ankles

o Rachitic Rosary enlarged costocondral junctions


o  Bone consists of protein matrix called osteoid and mineral phase , principally composed of Ca & Phosphate ,mostly in the form of hydroxyapatite

o  Osteomalacia is present when there is :

o  Inadequate mineralization of Bone osteoid

o  It occurs in children or adults

o Rickets is under mineralization of the cartilaginous epiphyseal growth plate resulting in excessive accumulation of un mineralized matrix (osteoid)

o Rickets is seen only a childhood because the growth plate exists only when the skeleton is growing

o Because growth plate cartilage and osteoid continue to expand

o But mineralization is inadequate , the growth plate thickens

o Also an increase in the circumference of the growth plate and the metaphysis

o  This increases bones width at the location of the growth plates .

o  Causing some of the classic clinical manifestations such as :

o  Widening of the wrists and ankles

o  There is softening of the bones that causes them to bend easily when subject to forces such as weight bearing or muscle pull

o  This leads to a variety of bone deformity

o Osteomalacia is under mineralization after growth is completed and is seen in adults

o     اصولا ریکتز در اثر کمبود ویتامین D است

o     ناتوانی در مینرالیزه کردن استئوئید استخوان در حال رشد است

o     تشکیل استخوان جدید توسط استئوبلاست ها شروع می شود که مسئول رسوب ماتریکس و به دنبال آن مینرالیزاسیون آن هستند

o     استئوبلاست ها کلاژن ترشح می کنند وبعد از آن تغییراتی در پلی ساکارید ها، فسفولیپید ها ، آلکالن فسفاتاز و پیروفسفاتاز رخ میدهدتا مینرالیزاسیون رخ دهد

o     فاکتور های متعددی بر رشد استخوان تاثیر می گذارند ، کلسیم ، فسفر ، فلوراید ، هورمون رشد

oدر ریکتز نقش رشد استخوان از تاخیر یا سرکوب رشد طبیعی غضروف اپی فیزی وکالسیفیکاسیون طبیعی استخوان ناشی می شود 

oاین تغییرات حاصل کمبود نمک های کلسیم وفسفر موجود در سرم میباشد

oسلول های غضروفی نمیتوانند چرخه طبیعی تکثیر ودژنراسیون خود را تکمیل کنند

oنتیجه این فرایند ایجاد یک خط اپی فیزی مضرس نامنظم در انتهای تنه استخوان است

oشکست در مینرالیزاسیون ماتریکس استخوان وغضروف  به ایجاد یک بافت نرم ، مضرس ، نامنظم منجر می شود

که مسئول بسیاری از ناهنجاری های اسکلتی ریکتز است

oریکتز ناشی از کمبود ویتامین D است میتوان به عنوان تلاش بدن در جهت حفظ سطح سرمی کلسیم در نظر گرفت

oدر غیاب ویتامین D کلسیم کمتری از روده جذب می شود

oبا کاهش کلسیم پاراتورمون ترشح می شود

oاین پدیده به حرکت در آمدن کلسیم وفسفر از استخوان منجر می شود بنابراین غلظت سرمی کلسیم حفظ میشود

oدر نتیجه غلظت پائین فسفر سرمی (به علت اینکه پاراتورمون باز جذب فسفر را از کلیه کاهش می دهد )

oافزایش فسفاتاز سرم ( ناشی از افزایش فعالیت استئوبلاستیک ) میباشد

o      آلکالن فسفاتاز سرم افزایش مییابد در شیرخواران کمبود پروتیئن یا روی ممکن است طبیعی باشد

o     هموستاز کلسیم وفسفر به جذب روده ای کلسیم وفسفر موجود در رژیم غذائی بستگی دارد

o     اگر محتوای روده اسیدی باشد

o     اگر شکر موجود در رژیم غذائی لاکتوز باشد

o      جذب کلسیم بیشتر میشود

o     فیتات موجود در حبوبات ممکن است جذب کلسیم را کم کند

o     آهن موجود در رژیم غذائی ممکن است جذب فسفر را کاهش دهد

o     اسید پالمیتیک واسیداستئاریک در رژیم غذائی جذب کلسیم را کاهش می دهد


o There are causes of rickets including :

o Vitamin D disorders

o Calcium deficiency

o Phosphorous deficiency

o Distal renal tubular acidosis

o Deficiency of metabolites of vitamin D:

o  a. Sunshine deficiency ;

o *  Inadequate exposure to sunlite

o * Factors preventing ultraviolet (UV) light penetration( industrial pollution , darkly pigmented skin, abundant clothing ) 

o b. Dietary vitamin D deficiency ;

o * Exclusive breastfeeding without vitamin D supplements

o * Food faddism (e.g. strict vegan diet usually combined deficiencies of vit D and Ca are seen

o c. Fat  mal absorption (usually causes deficiencies of both vit D and Ca)

o * Celiac disease

o * Extra hepatic  biliary  atresia

o * Short bowel syndrome


Vitamin D physiology

o  Vitamin D can be synthesized in skin

o  Depend on the conversion of 7-dehydrochlestrol to vitamin D3 (3-cholecalciferol ) by ultraviolet B radiation from the sun.

o  Vitamin D receptors are found on the kidney, intestine ,bone osteoblasts ,parathyroid gland.


Vitamin D deficiency

o  Vitamin D2 is available in the diet.

o  Cholecalciferol (vitaminD3)is naturally presentin human skin in provitamin form

o  Vitamin D2&D3are hydroxylated in the liver(25-Hydroxylation) to form (25-Hydroxylation) to form 25(OH)D3(calcidiol)

o  And again in the renal cortical cells (1-hydroxylation) to produce 1,25-(OH)2D3 (calcitriol)


o The main function of vit D-parathormone (PTH)-endocrine axis is to maintain the extra cellular fluid concentration of Ca & Ph (PO4) at appropriate levels to permit mineralization.

o The normal critical product of serum Ca X PO4 concentration, each measured in mg per deciliter , is  40 ; rickets occurs when the product of CaXPO4  less than  30

Clinical manifestations

o Craniotabes, a softening of the cranial bones

o Can be detected by applying pressure at the occiput or over the parietal bones .

o The sensation is similar to the feel of pressing into a Ping-Pong ball and the releasing

o Craniotabes, may also be secondary to;

o Osteogenesis imperfecta

o Hydrocephalus

o Syphilis

o It is a normal finding in many newborns but it typically disappears within a few months of birth . 

o Widening of the costocondral junction ,

o Results in a Rachitic Rosary ,

o This feels like the beads of rosary as the examiners fingers move along the costochondral junctions from rib to rib

Growth plate widening is also responsible for the enlargement at the wrists and ankles .

o The horizontal depression along the lower anterior chest known as ;

Harrison Groove occurs due to pulling of the softened ribs by the diaphragm during inspiration


o  There  is some variation in the clinical presentation of the rickets based on the etiology .

o  Changes in the lower extremities tend to be the dominant feature in X-linked hypo phosphatemic rickets .

o  Symptoms secondary to hypo calcemic occur only in those form of rickets associated with decreased serum Ca

o  Many children present because of skeletal deformity (Knock knee & Bow leg)

o  Others may have difficulty walking due to a combination of deformity & weakness

o  Other common presenting  complaints include F.T.T.& symptomatic hypo calcemic

o  Characteristic rachitic changes can be seen at other growth plates .

o  Decreased calcification lead to thickening of the growth plate

o  The edge of the metaphysis loses it sharp border, described fraying

o  Metaphysis changes from a convex or flat surface to amore concave surface , this is termed Cupping seen at the distal end of

o  Radus, ulna, fibula


Most cases of rickets are diagnosed based on the presence of classic X-Ray abnormalities . The diagnosis is supported by physical examination findings and history and Lab test results that  are consistent with specific etiology

A normal PTH level almost never occurs with vit.D deficiency and

o Suggests a primary phosphate disorder

o Ca deficiency may occur with or without vit.D deficiency

Nutritional deficiency

o  The initial evaluation should focus on :

o  Dietary history

o  Emphasizing intake of vitamin D & Ca

o  Rickets has occurred in children given product Soy milk but are deficient in vitamin D & or minerals .

Rickets is seen in infants who are exclusively Breast –fed.

Nutritional Rickets

o Lab test:

o Ca   low or N

o Po4  low for age

o Alkaline phosphatase  elevated

o PTH elevated

o Calcidiol decreased

o Calcitriol  decreased, N ,or elevated

o Urine generalized aminoaciduria

Mal absorption of vit. D

o  Is suggested by a history of :

o Liver or intestinal disease

o Undiagnosed liver or intestinal disease

o Should be suspected if the has GE symptoms

o Occasionally , rickets may be in Fat Mal absorption 

Renal disease

o A history of renal disease : proteinuria, hematuria, UTI is an additional consideration , given the importance of CRF as a cause  of rickets

Polyuria  may occur in children with CRF or Fanconi syndrome

Children with rickets

o May have a history of :

o Dental caries

o Poor growth

o Delayed walking gait

o Pneumonia

o Hypo calcemic symptoms

Family history given Genetic cause

Congenital rickets

o When there is severe maternal vit D deficiency during;

o  pregnancy

o Poor dietary intake of vitamin D

o Lack of adequate sun exposure

o Closely spaced pregnancies

o This newborn with rachitic changes



Secondary vitamin D deficiency

o inadequate absorption

o Decreased hydroxilation in the liver

o Because vitamin D  is fat soluble , variety of liver ,GE disease , liver disease , cystic fibrosis ,celiac , crohn disease ,mal absorption



o Children with nutritional vit D deficiency should receive vit D &

o  Adequate nutritional intake of Ca& Ph

o There are 2 strategies for administration of vitamin D

o With stoss therapy, 300,000-600,000 IU of vit.D are administered orally or IM as 2-4 doses over 1 day

o  The alternative is daily, high dose vit D

o  With doses ranging from 2,000 -5,000 IU /d over4-6 wk.

o  Followed by daily vit D  400 IU /d

o  It is important to ensure that children receive adequate dietary Ca &Ph

o   this is usually provided by milk, formula, & other dairy products