Babies arrive in the world with a surprisingly incomplete set of parts. Some structures that adults take for granted, like kneecaps and frontal sinuses, simply have not formed yet at birth. Others existed during early embryonic life and were deliberately dismantled before delivery. And a few systems, while physically present, are so functionally immature that they might as well be missing. The picture is more interesting than any single viral list of “missing baby parts” tends to suggest, because the reasons behind each absence are different and tell us something about how human development actually works.
Kneecaps That Aren’t Really There
The most commonly cited “missing” body part in newborns is the kneecap, or patella. This is both true and slightly misleading. Babies do have a structure sitting in front of each knee joint, but it is made entirely of cartilage, not bone. Because cartilage does not show up on a standard X-ray, a newborn’s knee looks like it has a gap where the kneecap should be. The bony patella begins to form when small islands of mineralized tissue, called ossification centers, appear within that cartilage pad. This typically starts between the ages of two and six, and the process is not complete until later in childhood. So when people say babies are “born without kneecaps,” what they really mean is that babies are born without bony kneecaps. The functional scaffolding is there from birth; it just has not hardened yet.
This distinction matters because it applies to a lot of the newborn skeleton. Babies are born with roughly 270 to 300 separate bone segments, many of which are still partly or entirely cartilaginous. Over the years, these pieces ossify and fuse, eventually producing the 206 bones of an adult skeleton. The kneecap gets all the attention, but the same principle holds for parts of the spine, the pelvis, and the ends of nearly every long bone in the body.
Bones Still Under Construction
Long bones like the femur and tibia develop through a two-stage process. During embryonic life, a primary ossification center forms in the shaft of each bone. But the rounded ends, the parts that form joints, develop their own ossification centers only after birth. These secondary ossification centers appear on their own postnatal schedule and are critical for the growth plates that let children’s bones lengthen over years.1PubMed Central. Periarticular Mesenchymal Progenitors Initiate and Contribute to Secondary Ossification Center Formation During Mouse Long Bone Development A newborn’s skeleton, then, is not just smaller than an adult’s. It is structurally different: softer at the joints, more flexible, and full of gaps that will fill in over the next two decades.
The sacrum offers another good example. In adults, the sacrum is a single fused triangular bone at the base of the spine. In a newborn, it is a collection of somewhere around 58 to 60 separate ossification centers that ossify and fuse in a highly organized pattern stretching from fetal life all the way to about age 30.2PubMed Central. Postnatal maturation of the sacrum and coccyx: MR imaging, helical CT, and conventional radiography A newborn’s sacrum is essentially a loosely connected stack of cartilaginous vertebral pieces. The coccyx, or tailbone, follows a similar trajectory from about eight separate centers.
Sinuses and the Empty Spaces in the Skull
Your skull is not solid bone. It is honeycombed with air-filled cavities called paranasal sinuses, which lighten the skull, warm and humidify inhaled air, and contribute to the resonance of your voice. Newborns, however, have almost none of this architecture. The maxillary sinuses (behind the cheeks) and ethmoid sinuses (between the eyes) are present as tiny rudimentary pockets, but they are so small that they are clinically insignificant. The sphenoid sinuses begin to develop in early childhood. And the frontal sinuses, the large ones behind the forehead, do not appear at all until around age six or seven, and they keep expanding well into adolescence.
Understanding this developmental timeline is clinically important. It is one reason true frontal sinusitis is essentially unheard of in toddlers: the sinuses in question do not yet exist. Pediatric sinus infections involve different anatomy than adult ones, and the rapid growth periods of these air cavities during childhood can create their own set of complications.3PubMed Central. Pediatric paranasal sinuses-Development, growth, pathology, & functional endoscopic sinus surgery
Teeth, Obviously, But Not So Obviously
Most people know babies are born without visible teeth, and most babies cut their first tooth around six months. But the tooth buds themselves are already present in the jawbone at birth, having formed during the second trimester of pregnancy. In rare cases, about one in every two to three thousand births, a baby arrives with one or two erupted teeth, called natal teeth. These are typically lower front incisors and are usually just normal teeth that erupted ahead of schedule, though they sometimes need to be removed if they are loose enough to pose a choking hazard.
What is genuinely absent at birth is the full set of permanent teeth. The buds for the adult teeth are forming inside the jawbone during infancy and early childhood, but the crowns and roots take years to develop. Wisdom teeth, the last to form, do not even begin calcifying until around age seven to nine, and they may not attempt to erupt until the late teens. So while it is technically more accurate to say babies are born without erupted teeth rather than without teeth entirely, the permanent dentition is legitimately absent for years.
The Embryonic Tail and Other Structures Lost Before Birth
Early in development, around the fourth to fifth week after conception, human embryos have a visible tail. This is not a metaphor or a vestigial bump; it is an actual protruding structure containing vertebral precursors and extending beyond the legs. By about the eighth week of development, the tail is gone. Research on how this regression happens has shown that caspase-dependent apoptosis, a form of programmed cell death, is the primary mechanism. The pattern of cell death in the human embryonic tail closely mirrors what happens in mouse embryos going through the same process.4PubMed Central. Spinal neural tube formation and tail development in human embryos
The process is tightly regulated by molecular signals. Elongation of the tail stops after certain growth-signaling molecules are dialed down in the tailbud around a specific developmental stage, accompanied by a burst of programmed cell death that clears out the progenitor cells responsible for building the tail.5eLife. Spinal neural tube formation and tail development in human embryos In extremely rare cases, a baby is born with a soft, boneless appendage in the tailbone region, sometimes called a “human tail” or vestigial tail. These are not true tails in the way a cat’s tail is a tail; they lack vertebrae and voluntary muscle. They are thought to result from incomplete regression of the embryonic structure.
The tail is not the only thing shed before birth. The lanugo, a fine coat of hair that covers the fetus starting around the fifth month, is largely shed into the amniotic fluid before delivery, though premature babies often still have patches of it. Webbing between the fingers and toes, present early in limb development, is removed by apoptosis during the first trimester. These are all examples of structures that are built as part of the developmental program and then deliberately eliminated.
A Circulatory System That Rewires Itself at Birth
In the womb, a baby’s cardiovascular system has plumbing that an adult’s does not. The most important example is the ductus arteriosus, a short blood vessel that connects the pulmonary artery to the aorta. Before birth, this shunt diverts blood away from the lungs, which are not yet being used for breathing. The placenta handles gas exchange instead. Within hours of birth, the ductus arteriosus constricts and begins to close. One study of healthy newborns found the median closure time was about 13.5 hours after delivery, with a range of roughly 8 to 19 hours.6PubMed Central. Closure time of ductus arteriosus after birth based on survival analysis
A second fetal bypass, the foramen ovale, is an opening between the two upper chambers of the heart. It allows oxygen-rich blood returning from the placenta to skip past the non-functioning lungs and go directly to the body. After birth, the pressure shift caused by the baby’s first breaths typically pushes a flap of tissue over this opening, functionally sealing it. In most people, this closure becomes permanent over the following months. In about a quarter of adults, however, the foramen ovale never fully fuses shut, leaving a small patent foramen ovale, or PFO, which is usually harmless and discovered incidentally.
So while a newborn is not exactly “born without” these vessels and openings, the baby is born with cardiovascular hardware that the adult body does not use. The ductus arteriosus and the foramen ovale are meant to disappear, and the transition from fetal circulation to postnatal circulation is one of the most dramatic anatomical changes a human body ever undergoes, all happening within the first day of life.
A Gut Without Its Microbiome
The adult human gut contains trillions of microorganisms that help digest food, train the immune system, and produce essential vitamins. A newborn’s gut, by contrast, is very nearly sterile. For decades, the “sterile womb” hypothesis held that babies develop in a germ-free environment and pick up their first microbes during birth and immediately afterward. More recently, some researchers challenged this idea, claiming they had detected bacteria in the placenta or amniotic fluid. But a careful assessment of the evidence has concluded that these findings are more likely explained by contamination during sample collection, and that the healthy fetal environment does not harbor a microbiome.7PubMed Central. A critical assessment of the “sterile womb” and “in utero colonization” hypotheses: implications for research on the pioneer infant microbiome
Colonization begins immediately at birth. Babies born vaginally tend to acquire bacteria from the birth canal, while babies born by cesarean section pick up skin and hospital-environment microbes first. Over the first few years of life, diet, environment, and other exposures gradually shape the gut community into something resembling an adult microbiome. The practical upshot is that a baby’s digestive tract, while structurally complete at birth, is functionally missing one of its most important components.
An Immune System Running on Borrowed Defenses
Newborns have immune systems, but those systems are profoundly immature compared to an adult’s. The adaptive immune system, which learns to recognize specific pathogens and build lasting defenses, is present but barely trained. Babies are known to have limited formation of the specialized immune structures needed to mount strong, long-lasting responses to vaccines and infections. This results in fewer memory cells and reduced levels of the more effective types of antibodies.8Nature. Sustained antigen delivery improves germinal center reaction and increases antibody responses in neonatal mice
To compensate, babies are born with a substantial supply of antibodies transferred from their mother across the placenta during the third trimester. This passive immunity provides temporary protection against many infections the mother has encountered. It is why premature babies, who miss out on some of this transfer, are at higher infectious risk. The borrowed antibodies gradually wane over the first several months of life, which is one reason the childhood vaccination schedule begins so early: the goal is to start training the baby’s own immune system before the maternal protection runs out.
Breastfeeding extends this borrowed defense through antibodies in breast milk, particularly secretory IgA, which coats the lining of the baby’s gut and respiratory tract. But these milk antibodies do not enter the baby’s bloodstream the way placental antibodies do. They work locally, at the mucosal surfaces where pathogens first make contact.
Sweat Glands That Cannot Sweat
Here is one that surprises most parents: full-term newborns have sweat glands, and in fact they have far more per square centimeter of skin than adults do. One study found an average of 414 active sweat glands per square centimeter on the thigh of newborns, roughly six and a half times the density found in adults.9PubMed Central. The response of the sweat glands of the newborn baby to thermal stimuli and to intradermal acetylcholine But despite this abundance, newborns are poor sweaters. Premature babies show virtually no sweat response to heat or chemical stimulation. Full-term babies can produce a modest sweat response, but it is significantly weaker than an adult’s.
The issue is not that the glands are structurally absent but that they are functionally immature. The maturation process depends on intact nerve connections from the central nervous system, and premature birth reveals how incomplete those connections still are. This functional absence has real consequences: newborns are poor at thermoregulation, and overheating is a genuine safety concern, especially for premature infants. The sweat response continues to develop over the first weeks and months of life.
Kidneys That Still Bear Fetal Marks
Newborn kidneys are structurally present and functional, but they look quite different from adult kidneys. During fetal development, each kidney forms as a collection of distinct lobules. In adults, these lobules have typically fused into a smooth bean-shaped organ. But in many newborns and young children, the fusion is incomplete, and the kidney surface retains visible indentations between the original lobules. This is called persistent fetal lobulation, and it is considered a normal variant.10MyESR / European Society of Radiology. The sound of kidneys: A non-musical ultrasound review of non-malignant renal findings in children
Fetal lobulation can occasionally cause confusion on imaging. A pediatric ultrasound that shows a bumpy kidney surface might initially raise concern for a pathological condition, but in young children, it is usually just a remnant of normal embryonic architecture that has not yet been smoothed over. Some adults retain fetal lobulation into adulthood with no ill effects. Still, newborn kidneys also have limited concentrating ability compared to adult kidneys, which is why young infants produce relatively dilute urine and are more vulnerable to dehydration.
Why So Unfinished at Birth
The sheer number of structures that are absent, incomplete, or non-functional at birth raises a natural question: why are human babies born in such an unfinished state? A well-known idea in anthropology, sometimes called the “obstetrical dilemma,” proposes that the answer lies in a conflict between the size of the human brain and the width of the birth canal. Bipedal walking constrains how wide the pelvis can be, while natural selection pushed human brains to grow larger. The proposed compromise was to shorten gestation so that the baby’s head is still small enough to fit through, resulting in newborns that are far more helpless than the offspring of most other primates.11PubMed Central. Metabolic hypothesis for human altriciality
More recent research has suggested the picture is more complicated. One alternative hypothesis proposes that gestation length is limited not by the pelvis but by the mother’s metabolism: at a certain point, the energy demands of the fetus simply exceed what the mother’s body can sustain, and birth is triggered. Whatever the primary driver, the outcome is the same. Human newborns emerge in a state of extreme dependency, with many organ systems still under active construction. Compared to a newborn horse, which can stand and walk within hours, or a newborn great ape, which can cling to its mother’s fur, a human baby cannot hold up its own head. The developmental finishing work that other species complete in utero must happen, for humans, during infancy.
Rare Congenital Absences
Everything discussed so far falls under normal development: parts that every baby is expected to be missing or to develop later. But there is also a separate category of body parts that are occasionally absent due to developmental errors. These congenital absences are rare and range from medically trivial to life-threatening.
Congenital absence of the gallbladder, for instance, is an extremely rare anomaly where the gallbladder simply fails to form during embryonic development. Most people born without a gallbladder never know it. The condition is often discovered incidentally during imaging or surgery for something else. Some affected individuals develop symptoms resembling biliary colic despite having no gallbladder, which can make diagnosis tricky.12PubMed Central. Congenital absence of the gallbladder in a child: a case report
On the other end of the severity spectrum, tracheal agenesis is a condition where the windpipe fails to form. This is extraordinarily rare and almost always fatal. It typically presents as an unexpected emergency during newborn resuscitation, when the medical team discovers that a breathing tube cannot be placed because there is no trachea to intubate.13PubMed Central. Failed resuscitation of a newborn due to congenital tracheal agenesis: a case report Even in the rare cases where a baby initially survives, the long-term prognosis remains poor.
Other congenital absences include missing kidneys (renal agenesis, which occurs in about 1 in 1,000 births for a single missing kidney), absent limbs or digits, and absence of the nerve networks that control intestinal movement. This last condition, where the nerve plexus in part of the colon fails to develop, produces what is now known as Hirschsprung disease, and it typically presents as intestinal obstruction in the newborn period.14Pediatrics. INTESTINAL OBSTRUCTION IN THE NEWBORN INFANT DUE TO AGENESIS OF THE MYENTERIC PLEXUS These rare absences are fundamentally different from the normal developmental gaps described elsewhere in this article, but they illustrate how much can go wrong when the elaborate choreography of embryonic development misses a step.