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Rickets
Get compression diagrams from PS case and 3 D
recomstrictions
Rickets is a metabolic bone disease caused by vitamin D deficiency
(VDD) and complicated by decreased total body calcium. It has been a
scourge worldwide that has spanned centuries. Lack of sun exposure
and poor diet led to the persistence of this medieval disease into the
modern era. This is illustrated from one of the many studies of rickets
done in the early 1900's when rickets was rampant. One study in
1920, showed 2/3 of all children living in Denver had rickets. It was
not until the 1930's that rickets was identified as a vitamin D
deficiency. Short stature, bowed extremities, the "rachitic rosary",
(bulbous flaring of the anterior bone-cartilate interface from abnormal
bone growth at the front or anterior of the bony ribs near the nipple
line (see image below), short leg and arm bones, large feet, and
knobby knees where the finding used in pre-modern medicine to
diagnose the conditon (see image below).

The rachitic Rosary in a small child and a third world family with never
treated rickets

With the development of x-ray technology around 1900, the imaging

findings associated with rickets were identified and included things
that could not be seen externally.
With imaging a variety of finding were identified with rickets.
Abnormal bone growth at growth plates led to the appearance of
irregular spicules, curly protuberances near the growth plate or
islands of calcified cartilage within the cartilage mass that only on
imaging appear like chip fractures, but are not fractures. These
lesions, the the so called classic metaphyeseal lesions or the CML's,

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were painless and came and went in days and changed almost on a
daily basis as calcium was deposited in the cartilage irregularly and
somewhat unpredicatably. These lesion had no characteristics of
normal fractures that are painful, show decrease range of motion and
go through a very predictable healing process.
Poorly demarked leading edges of calicum depostion in the growth
areas where the long bones elongate, were identified. The leading
edge of calcium deposition in long bones, the zone of provisioal
calcification (ZPC) was seen as undercacifeid and more tranparent on
x-rays.
Fraying (or irregularity) of the growth areas of all bones, sometime at
both ends, were noted due to irregular calcium deposition.
As bones grow in width, cartilage is layed down along the shaft of the
long bones or on top and bottom of flatter bones in the skull. This
occurs at a relatively steady rate in newborns who are growing fast.
The rated of cartilage development, outpaces the body's capacity to
deliver calcium to the new cartilage. The delay is due to VDD and
total body calcium deficiency (TBCD). Excess cartilage around the
shaft of bones builds up but is not seen on imaging since cartilage is
radiolucent (transparent to x-rays). The outer table of the bones, the
cortex, can be thin or almost transparent at time. With supplements,
increased sun exposure and improved calicum intake, resolution of
the rickets starts, and some calcium is deposited in the cartilage and
it becomes visible on imaging. This process results in new bone
formation called periosteal neostosis or periostitis, and appears as
smooth newly calcified cartilage along the shaft of the long bones. It is
an expected finding of rickets resolution. It is however similar to a
sign of healing occult longitudinal fractures of the long bones. The
lack of pain, a slightly irregular appearance from its traumatic
etiology, and normal use of the affected area rule out fracture and
supports the diagnosis of VDD.
Kupec ankle
Undercalcified bone (also refered to osteropenia, osteoporosis, low
denisty bone, thin bones) were identified on plain films and later with
special imaging tests. With DEXA scanning a special x-ray procedure
no longer widely available but easy to acquire, the deficency could be
quantified. It soon become clear that TBCD was common and the
correction of this, another factor in rickets resolution. VDD and TBCD
are the objective measures of rickets while radiology shows its bony
manifestation.

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These findings define the metabolic bone disease of VDD and
additional problems arise if total body calcium is low. Either condition
alone in newborns, can precipitate rickets
Early treatment
In the 1930's the government recommended sunbathing newborns as
sun exposure is the best, by far, spource of VD. UV rays hitting the
skin convert precursos to vitamin D.
In 1950's the government mandated that VD be added to mild and
campaign to drink milk for healthy bodies was successful. Milk still is
fortified with VD.
In the 1970's however aversions to the sun and fatty food (including
milk) started a trend that lowered VD and TBC levels that in 2006
were documented for the first time and created an awareness that a
new epidemic of VDD was upon us.
The entire process of bone formation progressed in a disorderly and
abnormal way due to the deficiencies. There is real potential for
change however with treatment including improved diet, vitamin
supplementation and more sun exposure.
VDD level can correct in weeks with high doses (i.e 50,000 units per
week) but calcium acquisition takes time (months) and rickets will not
resolve until both are fixed. Early changes in appearance can occur in
days to week and rickets can resolve completely over months, if
treated properly. With inadequate treatment it can persist and VDD in
older children is virtually epidemic as well and young females who are
pregnant were actually the first group to be identified as VDD in
multiple studies. These studies were intended to define VD status at
birth when the mother passes slightly lower values of VD than she
has1 and/or insufficient calcium to the fetus, since almost of all
mothers are calcium deficient themselves2.
VD moves dietary calcium from the blood into cartilage the precursor
of bone. The cells that make cartilage (osteoblasts) lay down cartilage
for new bone and are also part of repairing broken bones. The
abnroalities of new bone formatio manifest with fractures as well
causing abnormal and portacted healing. The healing of fractures is
both abnormal in appearance and strength. Lingering areas of
incomplete and delayed healing (new cartilage with only minimal
calcium) were identified early with the first x-rays and called Looser's
zones.

1
2

Bodnar
Cal defic

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The common condition of vitamin D deficiency (VDD) in pregnant
mothers and their babies, was identified in 2006 and is now
recognized as epidemic. It's relationship to both perinatal and
postnatal fractures is not in doubt3. Many VDD deficient fetuses are
exposed to extreme force during labor and are prone to fracture
during labor and deliveray and deformation of the weakened skull
bones are in part is responsible for approximately of all babies
being born with brain trauma manifesting as subdural hematoma.
The entire condition, present in about 85% of birthing mothers and
babies appears to be arbitrarily ignored by child abuse MD's who
seems focused on abuse regardless of evidence of metabolic bone
disease.
The commonality of the new epidemic of VDD was first identified by
Bodnar. He, and now many others, have shown that as a result of
inadequate diet, an aversion to exposure to direct sun (the primary
source of vitamin D) and the widespread use of sunscreen in the last
3-4 decades that 85% of women in Pittsburg were vitamin D and
calcium deficient at birth4. Furthermore whatever the mothers' state
of VDD and calcium was at birth is passed in slightly less than equal
measure to the child in utero and at birth. Ziegler (2010), Thomson
(2006), Ginde (2010), Holick (2006), Johnson (2010), Mansback
(2009), Cole (2010) and Merewood (2010)5 have all shown the same
thing, VDD is widespread and the bones diseased. This state can be
very problematic in newborns who have it.
Vitamin D deficiency (VDD) manifests in the bones as rickets, a
disease dating back to medieval times, now resurgent. The studies
cited above, should not be disregarded when the signs of bony rickets
are present regardless of vitamin D levels months after birth in the
baby. The low levels of vitamin D, rarely if ever measured at birth
routinely, begin to correct once the child is in the sun and getting
dietary supplements. This supplementation begins a healing cycle for
the bones that takes 6 month to a year to correct.
The Frieben baby, born prematurely, was to a reasonable medical
certainty vitamin D deficient at birth.

ED study of fx with VDD

Bodnar LM, et.al. High Prevalence of Vitamin D Insufficiency in

Black and White Pregnant Women Residing in the Northern United
States and Their Neonates, J. Nutr. 137: 447452. 2007
5
See studies in attached references folder

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Here is a table from a basic study containing the most common and
recognizable radiographic findings of infant rickets published in the
American Family Physician6.

The radiology expert consulted in this case is one of the most

preeminent pediatric radiologists in America and the head of Pediatric
Neuroradiology at Stanford, a very prestigious position. Dr. Barnes's
report (attached herewith) reports on the radiographic finding in the
Frieben baby. He notes the following which includes basic and other,
more sophisticated, but reliable signs of rickets that go beyond the
basics. The combination of the article and the report should reflect
common knowledge about rickets for a child abuse MD accusing
parents of abuse and appear to be ignored in the analysis of this case.
Dr. Barnes' findings included: [explanations by me in square brackets]

Heterogeneous mineralization throughout the entire

skeleton [uneven calcium deposition throughout the
skeleton]
Prominent irregular sutures of the brain and sutural
bones/fissures [extra bones and fissures of the skull
associated with VDD during gestation]
Lacunar skull changes/craniotabes, [irregular
deposition of calcium in the bones of the skull leading
variations in bone density within a single bone]
Bilateral anterior rib flaring/rachitic rosary [the oldest
recognized finding in rickets because it can be seen in
an exam and does not need lab or x-ray to identify]

Nield L, et. al. Rickets: Not a Disease of the Past. American Family
Physician. Volume 74, Number ; 2006

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Bilat old healing rib deformities L > R [the fractures

from birth]
R 9th has Looser zone7
Bone within bone in spine [again irregular calcium
deposition in bones]
Bilateral upper and lower metaphyseal changes
including irregularity, fragmentation, beaking,
spurring and L-J ring/bone collars [these are the classic
metaphyseal lesions discussed below that are
misdiagnosed as fractures]
Metaphyseal sclerotic changes [abnormal bone
densities at the growth plates]
Bilateral distal ulnar cupping, upper and lower
extremity cupping [finding known to occur in rickets at
the growth plates]
Cortical tunneling and periosteal reaction [more
esoteric findings present during a phase of resolution
of rickets]
Bilateral distal tibial and fibular tilting [angulated joint
spaces related to weakness and tendency for bones to
deform as they grow]
And old healing oblique L tibial fracture with periosteal
reaction [a pathologic fracture with healing reaction
that would older than 2 weeks and could date back to
birth due to slow healing with VDD]

Dr. Barnes conclusions, couched in the most conservative of terms

are:
"Most consistent with metabolic or dysplastic bone fragility
disorder in chronic healing phase with multiple deformities many
of which date back to birth. Strong consideration should be given
to neonatal VDD."
Craniotabes

Looser's zones are areas of abnormal healing at "fracture" sites that persist
for longer than normal since vitamin D and calcium are both required for
normal healing to occur. With VDD the amount of new cartilage around a
bone crack is excessive and forms a bulbous structure that takes more than
2 times normal the amount of time to heal. These "zones" were so common
that it was given a name: the Looser's zone, named after the radiologist that
identified it.
7

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No. There is no predictable relationship between rickets and alk phos,

serum calcium, or phosphate. VDD and imaging make the diagnosis. They
have tried to use the chemistries primarily to rule out rickets by
setting up criteria that were bogus (like the ones you are suggesting).
They can all be low, high or normal in the context of clinical rickets.
Very typical of the CA MD's to look for a trick to defeat rickets which
if validated is a huge problem for them since they rely on those
"fractures" so much to advance the abuse narrative when the primary
complaint might be considered weak on its own. Rickets is obvious both
historically, radiographically, epidemiologically and with respect to VD
level in the patient.
Total body calcium does not even get into the mix with these guys and it
is another diagnostic feature of VDD. And one that corrects slowly and
in a more reliable test. They won't do it. Instead they relay on their
tainted radiologists to "judge" that bone density is normal looking at
plain film. A study by Mulugeta (attached) showed how inaccurate that

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is. You need DEXA scanning to determine bone density which has a linear
relationship to the severity of rickets.
Total body calcium and VD must both be improving for rickets to resolve.

It should be recalled that the baby spent the first 9 days in the
hospital when no conventional signs of fractures were evident. In fact,
at no time was there any evidence of fracture noted clinically (i.e. by
examination). Anyone who has ever had a healthy bone break knows
how painful it is, how long the pain lasts and how much pain occurs
with movement of the fracture site for 2-4 weeks. The absence of any
pain with the many exams that took place in the hospital and during
post natal pediatric visits or handling by the family is on going proof
that no intentional infliction of fractures of an abusive nature
occurred and that all the findings in this case are signs of metabolic
bone disease (MBD): VDD.
The types of fractures seen in VDD are pathologic fractures (fractures
that can be caused by minimal forces, not expected to cause a
fracture: the defining quality of pathologic fractures). Labor in fact is
the force that causes many of the rib fractures seen in babies like the
Frieben baby, born with VDD, and the forces of labor are not a
minimal force. Compression of the chest from side to side (coronal
plane compression) forces an oval shaped chest to a round
configuration with all the force of uterine contraction and maternal
pushing at the end of labor, changing the shape of the chest. A nonVDD baby can tolerate these forces, but a VDD baby suffers cracks in
the ribs that occur on the inside surface as the ribs are not flexed, but
extended from the forces of labor trying to flatten the curved ribs, not
excessively bend them. The arms play a role in exerting extra force as
they usually are at the side of the newborn coming down the birth
canal and can be anywhere on the back, side or front of the rib cage
during the contractions. They arms cause extra deformity of the ribs
when they are caught in this squeezing and lead to a group of
fractures in a line as was the case here. A study by Garcia8 showed
that multiple rib fractures from severe external trauma cause lung
damage and none was noted in this case.
These cracks then stimulate the dysplastic (abnormal) healing
reaction that persists longer than normal and the characteristic
radiographic findings of the ribs that was evident in this case.
At the growth plates in the long bones, histologic studies9 have shown
that abnormal bone growth is also present there as well and was
8

Garcia F., et. al. Fractures in Children: A Marker of Severe Trauma.

Journal of Trauma. Vol. 30, No.6. 1990

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present in this case. In fact, this case was a textbook radiographic
demonstration of VDD manifesting in the long bones of the
extremities. These long bone abnormalities have been promoted by
child abuse authorities for many years as classic metaphyseal lesions
(CML), a finding they consider diagnostic of abuse. They speculate
they are caused by forceful bending of the extremities to the point
where the bones would break and chips would be knocked off at the
joints. The idea that this can occur in multiple places, all resulting in
similar findings which could only result from precisely applying
exactly the same force bone after bone, is not plausible. Metabolic
bone disease (MBD) is far more likely to account for the widespread
and symmetrical nature of these supposed fractures at so many sites,
all without evidence of injury clinically.
The metaphysis is the growth plate area, and these lesions related to
VDD (a type of MBD), are diagnosed as fractures when in fact the
represent the irregular deposition of calcium into new cartilage;
irregular growth related to VDD. The supposed fractures are pain free
and nontender and change from week to week especially when
vitamin D supplementation is concurrently being given. No callous
forms around at any time the essential matrix for a healing fracture.
These CML's are considered to be abusive chip or corner fractures by
child abuse MD's, while the histology of the areas have been studied
and shows that no fractures are present. Under the microscope they
reveal themselves to be just another variant of abnormal bone growth
and development specifically related to VDD. L-J rings seen in this
baby (and shown below) are another more subtle finding specifically
associated with VDD that was present and ignored.
The baby's ribs are shown below.

Raubenheimer EJ. Histopathologic Changes in Metabolic Bone

Disease. Adv Anat Pathol 2004; 11:3848

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L 9th rib with classic Looser's zone

A blow up of the CXR above shows smaller Looser type lesions, more
healed on L (at 3 arrows); old fractures most likely dating back to birth.
There was no history of chest wall pain at any time nor any respiratory
problems that would manifest if the lungs had been damaged after birth
as would be expected with 3 adjacent rib fractures in healthy bones.

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L-J ringanother classic rickets finding

With respect to the resolution of VDD, there is a substantial volume of
evidence that shows that even with vitamin D supplementation, it
takes time for rickets to correct since both adequate vitamin D AND
calcium must be present in sufficient quantities to allow the bones to
return to normal. Calcium in the baby is all dietary, so while higher
oral doses of vitamin D can correct vitamin D blood levels over time as
occurred in this case, the bony manifestation of VDD deficiency, the
rickets, persist for months.
In this case the baby was getting vitamin D from birth on in formula
called Neosure which had 70 u of Vit D per serving and later Similac
1-2 bottles per day with 60 units of vitamin D per serving.
Furthermore baby's multivitamins, which the baby got from birth on,
can have in most formulations 400 units per day of vitamin D. With
minimal, but additional vitamin D from breast milk, the baby could
have been getting more than 600 units per day to account for the
correction in vitamin D levels that were measured at 11 weeks.
Normal adult daily requirements are listed as 400 units per day and
this baby was 1/10th the size of an average adult.
Ziegler (2010)) tracked vitamin D levels in VDD babies for a year and
found this:

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0
Prematurity is likely to exacerbate all aspects of a VDD/rickets case
and this seems to have been ignored as well. The decision to ignore
VDD, even when the full array of radiographic findings are present, is
of great concern to those of us conscious of the serious legal
consequences of false and capricious accusations of abuse which are
so common now.
Before 1950 rickets was epidemic and widespread. The enormity of
the problem was addressed by the government by promoting drinking
milk for calcium and mandating that vitamin D be added to milk to
allow calcium in the diet to move into bone, the essential function,
among others, of vitamin D.
Rickets was studied extensively and many studies from that era
documented radiographic findings of rickets and others showed the
impact of rickets on rates of bone healing after fractures of any cause
and abnormal nature of the healing process that does occur.
Ineffective healing and calcium deposition and prolonged presence of
healing callous, up to twice as long, were documented by Copp as
early as 194410.
For a child abuse MD to dismiss prematurity, diagnostic findings of
rickets and to pronounce that that they subjectively feel these
10

Copp DH, Greenberg DM. Studies on Bone Fracture Healing- Effect of

Vitamins A and D 1. Journal of Nutrition. 1944

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etiologies are "inadequate" to explain "injuries", which may in fact not
be injuries at all, and then diagnose "abuse", with all its legal
ramifications, ignores the principle of evidenced based medicine.
Unfortunately, this occurs quite often and I believe occurred in this
case.
Lastly the skin findings referred to as "bruises" may in fact be an
allergic reaction or vascular autonomic instability. This form of
instability is neurologically mediated and is present in many newborns
and many premature newborns. The instability manifests as blood
vessels in the skin dilating from a variety of stimuli that can lead to
transient red markings that clear quickly and do not evolve through
the classic changes of bruising (red, to black and blue, to yellow/green
over 5-10 days).
This photo of the marking on the R arm of the Frieben baby are
remarkably similar in shape and size to the father's necklace the baby
was laying on just before these marks were noted for the first time.
Many less expensive pieces of jewelry and gold itself can cause mild
contact allergic dermatitis at times, which was not ruled out in this
case. There were no notes that these lesions evolved through any of
the other phases of a real bruise and the child abuse MD herself
stated that the "bruising cannot be definitely attributed to
nonaccidental trauma." Automatically assuming they are "bruises" is
another form of bias that can surface in these cases. These are "red
marks of unknown etiology" at the start and calling them "bruises"
immediately is used to imply abuse when abuse may not have
occurred.

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Note the similarity in width and the redness in areas most in contact with
the metal if the arm was resting on this necklace.

Adding further to the improbability of abuse is the very significant

lack of history of familial violence, no witnesses to violence, and no
reasonable probability that violence would occur in this family.
Studies done long ago and consistently disregarded, show that
nonviolent people are extremely unlikely to abuse their children in the
manner this family was accused of. Personal experience for each of us,
demonstrates that people we know are not prone to abuse their
children over common child care problems, and 50 low risk parents, in
a study by Kempe11, did not abuse their children in any way when
followed for 2 years after birth.
Kempe, one of the early promoters the notion of a scourge of child
abuse, studied low risk mothers and found that none of the 50 he
studied, who were characterized by him, through the application of
his own criteria, to be low risk, abused their children in any way. The
notion of loving people "snapping", the essential component in a dark
construct that is the basis of believing that loving people will break
the bones of their children over a wet diaper or crying, is unknown
and has never been proven through scientific study to be a reasonable
assumption. Yet it is an essential piece of almost every case of
11

Kempe H., et. al. Prediction and prevention of child abuse and
neglect. Child Abuse & Neglect, Vol. 1, pp. 45-58.

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physical abuse that is prosecuted. The average person does not know
anyone who would do that, and they in turn know no one who would
do that. The calculated odds of this happening are soon well above
1:1000 and in reality are much higher. Kempe couldn't find a single
case in his study of a low risk mother abusing their children. Without
witnesses or irrefutable evidence of abuse, such accusations reflect an
accusatory pathology in the accusers.
In this case there is no proof of abuse, just the medical findings, but
the medical findings are not diagnostic of abuse but in fact are most
consistent with VDD and MBD. When the nonviolent social history of
this young couple and the statements of the grandmother who lived
with them and never saw any violence, are integrated into the
analysis, it appears that speculating about a "snapping" phenomena
that is not evidenced based and does not have legal or medical merit.
Without independent witnesses to violence or a well documented
history of violence, drug use with stimulants and alcohol, or well know
risk factors12 for abuse, accusations of abuse in nonviolent families are
fundamentally implausible.
In spite of this, many child abuse MD's driven by beliefs in what
appears to be dogma, subjective opinions that are not evidenced
based, and peer pressure within the child abuse establishment, have
no hesitation to accuse apparently happy and loving parents of the
most heinous acts. Without witnesses and often in the face of
exculpatory social and medical evidence these accusations of abuse
are most likely to be wrong and fail to reach either the legal or
medical thresholds to be considered valid.
Submitted under penalty of perjury this 27th day of September 2010,
in Carmichael, CA.
Submitted electronically,
Steven C. Gabaeff, M.D., F.A.A.E.M.
Diplomat American Board of Emergency Medicine
Fellow of the American Academy of Emergency Medicine
I have been asked to write a brief report in the Frieben matter. Please
see my attached curriculum vitae for my qualifications and experience
in child abuse as both practitioner and clinical forensic consultant.
Introduction
In this case, and in many others I have consulted on, I have found that
faced with an infant with supposed "healing fractures", some quite old
Cavanaugh K., et. al. The murder of children by fathers in the
context of child abuse. Child Abuse & Neglect 31 (2007) 731746.
12

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and healed, and many that would date back to the neonatal period,
most child abuse experts inappropriately diagnose abuse as if it were
a default diagnosis. Abuse can be diagnosed in those cases when it
makes no sense based on social history, the lack of expected
concomitant physical findings of intentional abuse, and when the
findings noted are consistent with medical problems that cause the
precise signs that are being used to diagnose abuse. I believe that was
the case in this matter and it appears the child abuse MD's
themselves had some reservations with their diagnosis since these
used the term "probably" at times to qualify their diagnosis in the
records.
Vitamin D deficiency/Rickets
Calcifcation of the cartilage to conventional bone require both calcium
as a building block and VD to get it into the cartilage. Without either
bones grow and healing abnormaly