Fibrodysplasia Ossificans Progressiva or “Statue’s Disease”

Cindy Wilson Thumbby Cindy Wilson
BS, Dietetics and Nutrition

This article is published as part of Nutri Inspector’s scholarship application by Rebecca Noelle Donham who studies Biology and Philosophy at Sacramento City College.


Fibrodysplasia Ossificans Progressiva or “Statue’s Disease”–as it is also known–is characterized by a constant and extremely painful growth of bone in replacement of connective tissue, the muscles that control body movement, the ligaments that link the muscles to the bone, and the tendons that hold the skeletal system together (“Fibrodysplasia Ossificans Progressiva”; “Fibrodysplasia Ossificans Progressiva”). Fibrodysplasia Ossificans Progressiva is a chronic condition beginning in early adolescence of patients and progressively debilitating mobile ability until movement is rendered impossible (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). All organs, including the eyes, tongue, and brain, are left untampered (Giacopelli, Francesca, et al). Statue’s Disease hinders the patients ability to move while presenting no symptoms affecting the brain, thinking patterns, or sense of self (“Statue’s Disease Cracked”). Since patients are essentially trapped within their immobile body that this condition is also known as the “Statue Disease” (“Fibrodysplasia Ossificans Progressiva”).

Fibrodysplasia Ossificans Progressiva affects 1 in 2 million people worldwide (“Result Filters”). Currently, 3,300 people suffer from Statue Disease worldwide (Pignolo, Shore and Kaplan). Of these cases, 285 are known to be in the United States (“Fibrodysplasia Ossificans Progressiva”). The disease is non-discriminatory as it equally affects all demographics. Race, location, origin, and gender are not factors of Statue’s Disease (Matsumoto, Yoshihisa, et al.). Approximately 50% of cases have been found in men and 50% women with no distinct variations between ethnicities (“IFOPA”). The sole link between patients afflicted by Statue’s Disease is the mutation in the genome ACVR1 which is responsible for the growth of bone and cartilage (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis” ;”ACVR1 Gene”).

Cases have appeared throughout the world and detected as far back as early 17th century (Matsumoto, Yoshihisa, et al.). The most famous case occurred in 1973 under Dr. Guy Patin and his patient, Harry Eastlack Jr. (“Fibrodysplasia Ossificans Progressiva”;“Fibrodysplasia Ossificans Progressiva”-UCSF). Eastlack was finally diagnosed at the age of 20 when his vertebrae had completely fused together (“Fibrodysplasia Ossificans Progressiva”). He decided to donate his body to science in search for a cure (“IFOPA”). Eastlack passed away six days before his fortieth birthday from pneumonia (“IFOPA”). When his skeleton was prepared for scientific display, scientists discovered the majority of his bones were completely fused together (“OMIM Entry – # 135100 – FIBRODYSPLASIA OSSIFICANS PROGRESSIVA”; “FOP.”). In a normal skeletal system, bones connect to one another through tendons that deteriorate postmortem (after death) (“Statue’s disease cracked”). In Eastlack’s skeleton, and other patients affected with Statue’s Disease, bone replaces these tendons and holds the bones rigidly in place (“Fibrodysplasia Ossificans Progressiva” – UCSF). Mr. Eastlake’s skeleton currently resides in the Mutter Museum in Philadelphia and has become an enormous asset to researching scientists around the world (Pignolo, Shore, and Kaplan).

Although Statue’s Disease is not only painful but crippling as well, within its pain lies the key to cure many common ailments. By studying the ACVR1 mutation that occurs in patients with Statue’s Disease, scientists have concluded they are able to unlock information to rapidly heal bone-related injuries and diseases (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). These include, but are not limited to, treatments for broken and fractured bones and hip replacement surgeries, and a possible cure for osteoporosis (Matsumoto, Yoshihisa, et al). While Statue’s Disease is currently unknown due to its small number of victims, however, scientists predict in the near future, Fibrodysplasia Ossificans Progressiva will receive enormous recognition for its link to curing common ailments (Pignolo, Shore and Kaplan).

The Name Fibrodysplasia Ossificans Progressiva

Fibrodysplasia Ossificans Progressiva has many different terms commonly used by medical communities, supportive communities, the media, and across the globe. This condition is most commonly addressed as Statue’s disease due to its debilitating nature (“Fibrodysplasia Ossificans Progressiva.”). Other terms include Myositis Ossificans, Heterotopic Ossification, Progressive Osseous Heteroplasia, and FOP (“Fibrodysplasia Ossificans Progressiva: Clinical and Genetic Aspects.”). The official term, Fibrodysplasia Ossificans Progressiva, means “soft connective tissue [Fibrodysplasia] that turns to bone [Ossificans] progressively [Progressiva]” (“OMIM Entry – # 135100 – FIBRODYSPLASIA OSSIFICANS PROGRESSIVA; FOP”). All patients are born with Statue’s Disease, although painful symptoms called Flare Ups are not present until around the age of seven (“Frequently Asked Questions”). Because Statue’s Disease is progressive, symptoms of the condition will continuously become more severe as the patient ages (“Frequently Asked Questions”). The bone produced by Fibrodysplasia Ossificans Progressiva will not disappear and the condition will not be outgrown (“‘Statue’s Disease Cracked”).

Flare Ups

Victims of Fibrodysplasia Ossificans Progressiva will not grow bone all the time (“Fibrodysplasia Ossificans Progressiva: Clinical and Genetic Aspects”). Instead, bodies with Statue’s Disease undergo periods of time where soft tissue turns into bone or ossifies (“Fibrodysplasia Ossificans Progressiva.”). These periods of time are acutely painful and are known as “Flare Ups.”

Flare ups begin when lymphocytes and macrophages (special white blood cells that help the immune system) attack the muscles, including tendons, ligaments, and cartilage (“Fibrodysplasia Ossificans Progressiva: Clinical and Genetic Aspects”). Stem cells (special cells that have the ability to become any type of cell in the human body) divide and multiply to surround the areas where the soft tissue is attacked (“Frequently Asked Questions”). The stem cells then become cartilage – the type of tissue in the ears, the tip of the nose, and the windpipe as well as between bones as to allow movement, absorb shock, and prevent grinding of bones together (Butler, Lewis and Sheir 89). The cartilage then ossifies or turns into bone (“Fibrodysplasia Ossificans Progressiva”). This process of ossification causes noticeable tissue swelling on the outside of the body (“IFOPA”). The process of a flare up is identical to how healthy bodies heal broken or fractured bones and embryos form a skeleton (“IFOPA”). The type of bone and the manner in which bone forms in patients with and without Statue’s Disease presents no distinctions (“IFOPA”). It is the unusual location and timing of formation of the bone that is the distinction between patients with Fibrodysplasia Ossificans Progressiva (IFOPA”).

Flare ups typically begin in patients first decade of life, although the exact age of a first flare up varies without apparent cause among patients (“Fibrodysplasia Ossificans Progressiva: Clinical and Genetic Aspects”). The likelihood of experiencing a flare up highly increases when the patient’s immune system is weakened, which can be a result of illness, stress, or fatigue (Giacopelli, Francesca, et al.). The process of bone formation during flare ups may be rapid or gradual (Steele, Sarah, and Marilyn Hair). On average, flare ups last 6 to 8 weeks (Fibrodysplasia Ossificans Progressiva-“ UCSF). The length of flare ups vary from patient to patient, depending on the cause of the flare up, the muscles involved, and patient’s immune system (“Fibrodysplasia Ossificans Progressiva: Clinical and Genetic Aspects”). The time between “flare ups” also ranges from days to years, although length between flare ups will decrease as the condition progresses as the condition is degenerative (“Fibrodysplasia Ossificans Progressiva”; Fibrodysplasia Ossificans Progressiva-“ UCSF).


The condition of Fibrodysplasia Ossificans Progressiva displays very distinctive symptoms. According to researchers at UCSF, “95% of patients present valgus deviation [the atypical short and turned inward big toe] at birth” (“Fibrodysplasia Ossificans Progressiva“ UCSF). Discomfort to extreme pain while moving are early symptoms of Statue’s Disease which hint at future flare ups (Fibrodysplasia Ossificans Progressiva-“ UCSF). Flare ups- painful periods of time where the soft tissue turns to bone- and tumor-like swellings are important indicators of Statue’s Disease (“IFOPA”). The most alarming symptom of Fibrodysplasia Ossificans Progressiva is the visible bone protruding from the body later on in the patient’s life (“ACVR1 Gene”).

General and chronic symptoms of Statue’s Disease include tissue swelling, joint stiffness, body discomfort, inflamed swellings- typically on the back, shoulders, neck, and head- and occur before a patient’s first flare up, as well as periods of time between flare ups (“Result Filters”).

Rare symptoms of Fibrodysplasia Ossificans Progressiva include fever during flare ups and bone fusion in big toe or toes at birth (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”).

According to Dr. Kaplan, a prestigious M.D. specializing in bone and joint surgeries, if symptoms of Statue’s Disease are present in patients by age 7, it is most likely that by age 15, the patient will lose mobility of upper limbs(“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). By age 30, the patient is predicted to be confined to a wheelchair with a life expectancy of another ten or so years (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”).


Although almost 80% of Statue’s Disease cases are misdiagnosed, diagnosing Fibrodysplasia Ossificans Progressiva is very easy to do because of its distinctive symptoms that are visibly noticeable early on in life (Pignolo, Shore, and Kaplan).The earliest tell-tale symptom of Statue’s Disease is the malformation of the big toe or toes (“Fibrodysplasia Ossificans Progressiva”-UCSF). One or both toes of patients with Fibrodysplasia Ossificans Progressiva are often shorter than the rest and turn inward to the other toes, a symptom call valgus deviation (“ACVR1 Gene”). Over 95% of patients diagnosed with Statue’s Disease present contortions to one or both large toes, making this symptom one of the easiest ways to detect Statue’s Disease early on in life (‘Fibrodysplasia Ossificans Progressiva”). The severity of malconformation of a patient’s toe varies dramatically, although there is no evidence to suggest the differences of toe structure link to the severity of other FOP symptoms or lifespan (“Result Filters”).

According to the International Fibrodysplasia Ossificans Progressiva Association, “Rather than crawl on their hands and knees, most kids with FOP scoot on their buttocks; then get up and walk. The reason that most cannot crawl is because the facet joints in the back of the neck have not formed properly or have fused, thus limiting movement” (“IFOPA”). Like the malformation of the large toe at birth, the difference in mobility in infancy is a tell-tale sign of Fibrodysplasia Ossificans Progressiva (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis.”).

During childhood, very distinctive symptoms of Statue’s Disease come to light (Fibrodysplasia Ossificans Progressiva.”). At around the age of seven, patients with Fibrodysplasia Ossificans Progressiva will note chronic stiffness and discomfort with possibility of large lumps in the upper and lower back regions, shoulders, and neck (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). As the child grows, so will the severity of Statue’s Disease, with discomfort progressing to the hips, knees, and elbows (Steele and Hair 8). As the condition progresses in children, flare ups will begin to occur (“Fibrodysplasia Ossificans Progressiva”-UCSF). Tumor-like swellings will begin to appear upper and lower back regions, shoulders, head, and neck (“Fibrodysplasia Ossificans Progressiva.”). “The swellings will go down after some time, and reveal a ‘hard bump,’ which is the newly formed bone” (“IFOPA”). Over time, the patient will be unable to bend limbs, move with ease, or stand in an erect position (“Fibrodysplasia Ossificans Progressiva”-UCSF). As the condition progresses, Fibrodysplasia Ossificans Progressiva bones will become clearly visible in the patient’s body from the human eye (Giacopelli, Francesca, et al).


Because Statue’s Disease is one of the rarest diseases in the world, it is not well known, even within the medical community. Its unawareness often leads to misdiagnosis. In fact, “over 80% of cases are misdiagnosed in the United States” (“Fibrodysplasia Ossificans Progressiva”-UCSF). The misdiagnoses often lead to painful and invasive procedures like biopsies (“Fibrodysplasia Ossificans Progressiva” – UCSF). These invasive procedures often induce trauma and trigger flare ups, exacerbating the symptoms of Statue’s Disease and leading to more painful bone formation (Fibrodysplasia Ossificans Progressiva” – UCSF).

Common misdiagnosis include various types of Cancer, aggressive juvenile fribromatosis–which creates large swellings like those of Statue’s Disease, although instead of bone, cells called fibroblasts grow in muscle, tendon, and ligaments- and progressive osseous heteroplasia- a rare disease similar to Fibrodysplasia Ossificans Progressiva in which bone forms within muscle tissue and skin (“Genes and Mapped Phenotypes”; “Thoracic Insufficiency Syndrome”). However, Scientists are hopeful that as more awareness of Fibrodysplasia Ossificans Progressiva spreads, the less misdiagnosis will occur (“IFOPA”).

Systems Affected​

Statue’s Disease affects solely physical traits (“Fibrodysplasia Ossificans Progressiva”). The brain and cognitive patterns or how the patients thinks are completely unaltered (“Fibrodysplasia Ossificans Progressiva”-UCSF). Patients afflicted by Fibrodysplasia Ossificans Progressiva can hear, see, taste, touch, smell, learn, socialize, and think just as healthy individuals (Steele and Hair 12). Although physical immobilization hinders some aspects of life, most children with Statue’s Disease receive education of some kind and can live relatively normal lives with some modifications to take into account the physical immobilization (Matsumoto, Yoshihisa, et al).

Additional systems unaffected by Statue’s Disease include smooth muscles including the heart, the diaphragm, tongue, the eyes, and all internal organs (Butler, Lewis and Sheir 48). Reasons why Statue’s Disease spares smooth tissue is currently underway in research labs around the world (“Genes and Mapped Phenotypes”). Scientists seem hopeful about finding an explanation, although they are forced to work with limited tissue samples because each sample taken triggers a flare up and the formation of bone quickly follows (Matsumoto, Yoshihisa, et al).

Physically, victims of Statue’s Disease will gradually decline (“Result Filters”). As a toddler, patients will have few signs of Fibrodysplasia Ossificans Progressiva’s affect (Fibrodysplasia Ossificans Progressiva”). Within their first decade, patients will notice tumor-like swellings in their back, shoulders, and neck regions accompanied by pain and difficulty moving (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). At this stage, flare-ups begin, affecting the immune system so it attacks soft tissue (Matsumoto, Yoshihisa, et al). After the soft tissue is affected, dormant (“sleeping”) stem cells will be awoken to fill in the space where the tissue used to be and then ossify or turn into bone (“Fibrodysplasia Ossificans Progressiva”). As the patient progresses, so will the condition on the body (Fibrodysplasia Ossificans Progressiva”). The flare-ups will spread across the body, from the shoulders to the limbs and finally the cranium (“IFOPA”). The ossification of the body will leave the patient unable to move limbs, neck, fingers, and eventually mouth (“Fibrodysplasia Ossificans Progressiva”-UCSF). Because of this, most patients are confined to a wheelchair by the second or third decade of life (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Once the mandible (jaw) has been affected, the patient will be unable to chew food and receive nutrients as a healthy patient (Pignolo, Shore, and Kaplan). Often times a feeding tube is installed by the fourth decade (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Patients unable to have an alternative way of gaining nutrients other than consumption will experience sudden weight loss, malnutrition, and, if left untreated, death (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Flare ups will continue to occur, often times more frequently than before, and the majority of the soft tissue will be ossified by the fourth or fifth decade of life (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Around this time, the thorax (chest) becomes unable to support normal respiration in the lungs due to bone growth limiting the expansion of the lungs to receive enough air (Butler, Lewis, and Sheir 12; “Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Once the throat has been affected by Fibrodysplasia Ossificans Progressiva, the patient experiences Thoracic Insufficiency Syndrome or the inability to breath properly because the lungs are unable to expand in the way a healthy chest can (“Thoracic Insufficiency Syndrome”). Once the patient passes–like all humans–bone growth, including Statue’s Disease bone, stops.

Life Span​

In 2010, scientists studied mortality registers of individuals whom passed due to complications resulting from Fibrodysplasia Ossificans Progressiva to determine the most common cause of death and the average life span of those with Statue’s Disease. During a 33 year period, 60 individuals had passed away- 30 female, 30 male (“Result Filters”). “Together, these registries comprise >90% of all known patients with this condition in the world. We noted the sex, dates of birth and death, and the cause of death for each individual. We verified the cause of death with extensive medical records, when available. We also collected date of birth, current age, and sex information for each living patient member of the International Fibrodysplasia Ossificans Progressiva Association” (“Result Filters”). The age of death in these 60 individuals was 3 to 77, averaging a mortality age of 48 (“Result Filters”). Taking into account the number of living patients- which numbers 371- with the 60 deceased patients from the last 33 years, the estimated, average age of mortality is 56 (“Result Filters”).The cause of death for the 60 deceased individuals resulting in 48 individuals- 24 female, 24 male- unable to be determined due to insufficient information on the registries (“Result Filters”). The median age of the 48 unknown individuals was 40 years old (“Result Filters”). From the other 12 individuals, 54% passed from thoracic insufficiency syndrome with a median mortality age of 42 (“Result Filters”). “For all sixty patients, the median age at the time of death was forty years (range, three to seventy-seven years)” (“Result Filters”). The researchers concluded complications of Fibrodysplasia Ossificans Progressiva significantly limit the average lifespan of its victims, predicted to be only 56 years of age (“Result Filters”).


Because Statue’s Disease is so rare, little is known about its mysterious condition. As of 2006, researchers discovered Fibrodysplasia Ossificans Progressiva is a genetic condition caused by a mutation (“Statue’ disease cracked”; “Fibrodysplasia Ossificans Progressiva.”). The mutation is believed to be linked to the mutation of the ACVR1 gene (“Genes and Mapped Phenotypes”). The ACVR1 gene is a bone morphogenetic protein (BMP) type I receptor, which is responsible for bone growth (“Fibrodysplasia Ossificans Progressiva”-UCSF;”Genes and Mapped Phenotypes”). Scientists have noted the mutation appears to result in a single base change of a single amino acid called R206H (“Genes and Mapped Phenotypes”). Scientists believe the condition is so rare because the chances of a mutation this specific amino acid are so slim (“Statue’s Disease Cracked”). Additionally, Fibrodysplasia Ossificans Progressiva equally affects all ethnicities and genders, verifying the possibility of the ACVR1 mutation since all ethnicities and genders have it as well (Giacopelli, Francesca, et al.).

Fibrodysplasia Ossificans Progressiva is rarely inherited and passed from parent to child (“Fibrodysplasia Ossificans Progressiva”-UCSF). The majority of children born with Statue’s Disease have no familial history of the believed mutation (“Fibrodysplasia Ossificans Progressiva”). “The chances of birthing a child with Fibrodysplasia Ossificans Progressiva is approximately 1 in 2 million”(“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Although very few people with Fibrodysplasia Ossificans Progressiva choose to have children, limited research shows parent with Statue’s Disease have a “50% chance of birthing a child with Statue’s Disease” as well (“Fibrodysplasia Ossificans Progressiva”-UCSF).

Little more is known about the cause of Fibrodysplasia Ossificans Progressiva, however multiple researching teams around the world are searching for answers (“IFOPA”). The University of Pennsylvania School of Medicine, the only laboratory in the US dedicated to FOP research, is currently looking for answers after their discovery in 2006 about the ACVR1 gene (“IFOPA”). The Department of Orthopaedic Surgery, NIH/NIAMS, and Orthopaedic Research and Education Foundation, as well as many smaller organizations currently search for the root of Statue’s disease as well (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). All are hopeful to find a cause to Fibrodysplasia Ossificans Progressiva, to find a cure (“IFOPA”).

Future Treatments and Cures​

There is little known about the complexity and anomaly that is Fibrodysplasia Ossificans Progressiva. Its rarity makes it unknown, but its uniqueness may bring it to light.Currently, there are no cures for Fibrodysplasia Ossificans Progressiva (“Fibrodysplasia Ossificans Progressiva”). “While the bone formed by the condition can be surgically removed, surgical intervention often results in a worsening of the condition. New bone will grow back and further impair mobility” (“IFOPA”).

Additionally, treatments for Statue’s Disease only treat the symptoms and not the condition. Medication to relieve pain and inflammation are most commonly used (Matsumoto, Yoshihisa, et al). Scientists highly suggest all Fibrodysplasia Ossificans Progressiva patients seek the consolation of a physician to ensure the best possible treatment of symptoms and pain management (“IFOPA”). The most effective treatment, however, is simply to minimize triggers of flare ups caused from bumps, stress, or illness (OMIM Entry – # 135100 – FIBRODYSPLASIA OSSIFICANS PROGRESSIVA; FOP”).

Despite the lack of current treatment and cures, medical professionals are hopeful to find a cure in the near future. Major breakthroughs as to the root of Statue’s Disease occurred in 2009 and since then, researchers have been slowly chipping away at a cure (“‘Statue’ disease cracked”). “Over 1.5 million dollars is annually donated to the search for a cure” (“Fibrodysplasia Ossificans Progressiva.”). Of the 1.5 million, 75% of funds are raised by friends and family of victims with Fibrodysplasia Ossificans Progressiva (“IFOPA”). The additional “25% is raised by organizations such as NIH/NIAMS, and Orthopedic Research and Education Foundation” (“IFOPA”).


lthough Fibrodysplasia Ossificans Progressiva is a devastating condition, within it lays the key to cure other ailments. By understanding Statue’s Disease, scientists say, they will harness the knowledge that could be applied to treatment and cures for ailments such as broken and fractured bones, hip replacement surgery, and osteoporosis (“IFOPA”). Researchers are currently assessing in further depth the ACVR1 gene whose mutation causes Fibrodysplasia Ossificans Progressiva to gain insight on ways to decrease the time bone formation requires as to possibly heal bones faster (“Statue’ disease cracked”). Once researchers understand Fibrodysplasia Ossificans Progressiva, professionals argue, they will be able to cure it—and other bone diseases (“OMIM Entry – # 135100 – FIBRODYSPLASIA OSSIFICANS PROGRESSIVA”).

In a way, flare ups from Statue’s Disease are an additional layer of protection for each patient. Flare ups result mainly out of physical trauma, upcoming illness, or stress (Giacopelli, Francesca, et al). The healthy body would simply take the stress of the external or internal problem without developing dramatic alterations to the body. Bodies with Fibrodysplasia Ossificans Progressiva, however, generate additional bones, perhaps to defend internal organs from believed stress. For this reason, Fibrodysplasia Ossificans Progressiva may not be a negative condition, but a stepping stone to a possible branch of human evolution—an evolution of a stronger, larger, denser, and forever-growing skeleton.


Fibrodysplasia Ossificans Progressiva or Statue’s Disease is an extremely rare and debilitating condition where soft tissue turns to bone (“Fibrodysplasia Ossificans Progressiva.”). Patients are born with the condition, although dramatic symptoms -such as flare ups- are not present until an average age of seven (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). As the patient grows older, the condition worsens and flare ups become more common (Fibrodysplasia Ossificans Progressiva-“ UCSF). The majority of the patient’s life will be confined to wheelchair and life expectancy in between the fourth and fifth decade (“IFOPA”). However, as devastating as the condition is, it holds the key to cure many other ailments such as Osteoporosis (“Fibrodysplasia Ossificans Progressiva: Mechanisms and Models of Skeletal Metamorphosis”). Scientists are confident that with the increased media from the link between Fibrodysplasia Ossificans Progressiva and a cure for Osteoporosis, will come an increase of funding and research to cure Statue’s Disease itself.​


About Author

Cindy Wilson Thumb
BS, Nutrition & Food Science | Connect with on LinkedIn
Cindy Wilson

Hello, I am Cindy, and this a website where I inspect everything related to nutrition and a healthy lifestyle. I have a BS in Dietetics and Nutrition (Kansas State University) and have completed a dozen specialty courses related to nutrition, biochemistry, and food science. I am open to learning more, but foremost I would like to share all my knowledge with you.

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