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Tortoise Shell Deformities: A View from the Inside

Updated: Apr 1

Why avoiding growth deformity is so very important

A typical example of not only raised scute growth (commonly known as 'pyramiding') but also of carapace depression in the pevic area. This latter is the result of weakened carapace bone being deformed by the powerful muscles that are attached in this region.

It is often said that a 'picture is worth a thousand words'. Here we have a number of pictures that illustrate graphically the difference between typical wild tortoises and those suffering from poor diet and environment in captivity. In wild tortoises, the bone density tends to be really excellent. Growth is normally far slower than seen in many captive-raised animals due to cyclic (not constant) feeding patterns, the dietary composition is 'correct' for that species, there is an optimal level of exposure to natural UV-B (essential for the correct functioning of the vitamin-D metabolism), temperatures (also critical for the correct functing of the vitamin-D metabolism) and humidity are also all within the 'correct' parameters and in addition, more subtle factors such as natural 'wear and tear' are present that has the effect of preventing unhealthy and unnatural buildups of over-thickened keratin. All of these thing play a vital role in producing the typically strong, healthy growth that we almost invariably see in wild tortoises. It is very important to stress that we need to consider all of these factors not in isolation, but collectively and holistically, as if any single one of them is not right this can manifest in developmental problems. This is especially so for juveniles during early-phase growth, where problems that occur here are likely to remain for life. Some of the mechanisms involved in producing (or preventing) such problems are quite complex. We cannot hope to cover them in a brief article such as this, but we have analysed them in detail elsewhere. This is merely a short introduction to what goes on 'under the shell' in such cases. The wild carapaces shown here are all from either road casualties or predator attacks. The deformed, captive examples were obtained following veterinary autopsies after the tortoises died as a consequence of their condition. No living animals were harmed. We have added notes to each image to explain some of the different classes of deformity that are commonly encountered, together with notes on causes and prevention.

There are a number of important concepts that it is critical to understand at the outset. One of these is that living bone tissue is not 'fixed and hard' but is in fact, 'plastic'. It is also in a state of flux, and can both gain AND LOSE calcium and other minerals. It is live tissue in a constant state of change.

This is at its most evident when a tortoise just hatches. The carapace bones are still highly pliable and the juvenile is still 'folded'. Over hours and days this gradually straightens out, but it is important to recognise that right up until the bones full stabilise and ossify, as the tortoise attains adulthood, some degree of plasticity remains. It is just not as obvious.

As a juvenile first emerges from the egg, the pliable and soft nature of the skeleton and bones of the carapace are at their most obvious. This gradually straightens out and the bones become more resistant, however, this property does remain to a considerable extent until the tortoise ceases growing and attains adult size. It merely becomes a much slower, and much less obvious process.

We apologise for the descent into some unavoidable technical jargon here, but this is a very valuable quote, worth taking the time to read and think about. It is from a paper called "Plasticity and toughness in bone" by Robert O. Ritchie, Markus J. Buehler, and Paul Hansma (June 2009 Physics Today).

"Results suggest that permanent deformation, or plasticity, in bone occurs from multiple, concurrent deformation mechanisms that are active at all hierarchical levels. To appreciate the deformation mechanisms in bone, consider again its different structural levels. Individual collagen molecules deform by stretching and unwinding due first to entropic and then to energetic mechanisms that involve H-bond breaking. In collagen fibrils, molecular stretching competes with intermolecular sliding and the breaking of both weak and strong bonds between tropocollagen molecules. Those sliding motions enable bone to endure large plastic strain without suffering a catastrophic brittle failure"

Tortoises and turtles are absolutely no different from dogs, cats or humans in this respect. It is very important to get this out of the way as there is a widely held, but entirely mistaken, belief among many tortoise and reptile keepers that they are completely different in this respect. They are not. The exact same 'rules' of nutrition and physiology apply to tortoises and turtles as apply to mammals. Their skeleton (the most obvious part of which is the carapace) responds in exactly the same way as mammals to dietary deficiencies or imbalances, and to physical stresses. Where they do differ is that because of their unique structure, these physical stresses occur at different points, however. So, in a human with rickets (which is a condition that affects bone development in children), the effects are bone pain, poor growth and soft, weak bones that can lead to bone deformities, typically in the longer bones of the legs caused by gravitational downward pressures and by the 'pull' of muscles ( causing the classic 'bowed legs' of rickets) . Adult humans can also experience a similar condition, which is known in this case as osteomalacia ('soft bone disease'). In adults, symptoms can include spinal, limb, or pelvic deformities. The primary causes are, yet again, vitamin-D deficiencies often in combination with calcum deficiencies or calcium-phosphorus imbalances due to either direct dietary causes, or some other serious underlying medical condition such as renal damage that can also adversely affect these metabolisms. Another term for these conditions is nutritional secondary hyperparathyroidism (NSHP).

In this clip (no sound) you can see clearly how the keratin scute growth is deforming the bone beneath, and just how soft and 'rubber-like' the skeleton has become.

Inadequate levels of calcium in the diet cause the parathyroid gland to produce too much parathyroid hormone (PTH). This causes the body to try to source calcium frrom the existing 'stock' within the bones. As a result, they become soft and rubbery and develop lesions.

One effect of osteomalacia is that the bones are far too soft, and easily deform. In this case (a young Stigmochelys pardalis, Leopard tortoise), there is pelvic region depression, combined with severe 'pyramiding', and - internally - severe distortion (nutritional kyphosis) of the spine. This tortoise had been raised on a diet far too high in phosphorus, deficient in calcium, and with inadequate access to effective UV-B. In addition, the keratin had been 'baked' under too-close heat lamps in a totally unsuitable enclosed vivarium system.

Another very common manifestation of bone disease in tortoises that is implicated in such cases is also sometimes known as nutritional fibrous osteodystrophy. It too results from a dietary imbalance of calcium and phosphorous and/or a deficiency in vitamin D (which in turn, in herbivorous reptiles, is typically related to a lack of UV-B). This particular form is most commonly observed in young animals undergoing rapid growth. Indeed, all forms of MBD are closely associated with rapid growth, as noted in the MSD Veterinary Manual "Affected reptiles are generally rapidly growing herbivorous and insectivorous lizards and chelonians". A particular feature of this condition is increased osteoclastic bone resorption combined with an increase in fibrous connective tissue. In practice, the bone appears thickened, deformed, full of lesions and - as it has been vividly described - "rather like Gruyere cheese", "like a honeycomb" or "shot full of holes". In this form of bone disease, minerals that should be used to build bone density and strength are actually lost back into the bloodstream ('resorption'). The process involved is quite complex but typically includes the activity of parathyroid hormone (PTH), in response to a fall in the level of serum calcium.

An extreme example of an American box turtle (Terrapene carolina triunguis) with a carapace severely deformed as a result of nutritional fibrous osteodystrophy. The normal, smooth, dense bone of a healthy turtle is almost non-existent, instead replaced with this grossly thickened, fibrous and porous tissue. The cause was a diet based upon commercial 'pellet foods', excessive amounts of fruit, and animal foods such as waxworms and crickets in great excess. This results in a devastating lack of calcium and an excess of phosphorous.

Internally, the results are just as dramatic. The entire skeleton will be affected, and the consequences are not limited to merely the carapace (though that is the most obvious). Other common effects include fractures of the jaw and limbs. There is little doubt that this condition will result in pain and suffering. Let's take a look at what affected bones look like, internally, compared to the bones of wild, healthy tortoises.

This is a normal, very healthy plastron of a wild tortoise. The bone is incredibly smooth and has outstanding density. This tortoise had a natural diet of wild vegetation, an adequate calcium intake, and natural UV-B.

This plastron, however, which is from a tortoise of similar age tells a completely different story. This tortoise was kept as a pet and fed on 'supermarket salads', with additional fruit content, These are the classic signs of nutritional fibrous osteodytrophy, with porous, weak bones,due to severe demineralisation.

Let's take a look at some other comparative bone tissue samples. These are incredibly instructive in showing us exactly what is going on 'inside' these animals, and just how serious and devastating these conditions really are. This is from the 'bridge' section of a wild tortoise carapace. Note the very good bone density. This translates directly into bone strength and resiliance, and also suggests that the blood calcium and phosphorus levels were in a good balance with adequate UV-B/D3.

Compare directly to another sample from a carapace, but this time from a captive-raised tortoise where commercial 'pellet' foods, salads, fruits and similar items were the main dietary components. The weakened, 'fibrous' nature of the bone tissue, filled with lesions, is very obvious here. The keepers do not typically even realise how bad things are until the tortoise suddenly declines and dies.

This is the outside view of quite a typical looking captive-raised tortoise. In fact, although there is visible deformity here, most of us will have encountered far, far worse! This is, indeed, 'pretty average' compared to many. Note, however, the depression just above the pelvis - typical of bone distortions and deformity resulting from internal muscular attachments. There is also 'pyramiding' which is especially obvious along the veterbral scutes.

Now, let's take a look at what this looks like from the inside, remember that this tortoise does not look 'too bad', externally.... internally, however, the damage is fully revealed. Massive skeletal deterioration along the spinal-veterbral region, multiple lesions, fibrous tissue replacing what should be solid, strong bone and absolutely no comparison to what is found in wild, healthy tortoises. Tortoises like this usually give few signs just how bad things are, and may display no easily recognised signs of distress or pain.

As a reminder, this is a 100% wild, extremely healthy Testudo graeca graeca female in natural habitat in southern Morocco. Note how beautifully smooth the carapace is, totally free of all deformities...

It is critical to note that in some cases both osteomalacia and fibrous osteodystrophy will occur not only separately, but together. It is also vitally important to understand that in humans with these conditions both are reported to result in SEVERE BONE PAIN. Humans can tell us this. Tortoises cannot. Therefore, suggesting that these conditions are "only cosmetic" or "don't really matter" (claims sadly often seen in uneducated tortoise groups on social media) is not only wrong but in all probability, hideously inhumane and resulting in unrecognised chronic pain and suffering.

These conditions should never be minimised. They are extremely serious and have irreversible consequences. Preventing them at source is therefore critical.

To understand just how serious this is, here we have a two-year old Centrochelys sulcata (African spurred tortoise) entirely typical of examples kept in a vivarium, provided with completely inadequate UV-B, and maintained on a totally unsuitable diet based on 'supermarket' salads, vegetables, commercial pellets, and fruit. It displays the full range of symptoms that we see in tortoises with a combination of these conditions.

Internally, the condition of the skeleton is absolutely shocking. There is widespread demineralisation, there are massive lesions, and the bone carapace 'plates' are reduced and paper-thin.

One of the most common forms seen involves what many keepers call 'pyramiding':

Misinformation on this subject is legion. There are entire groups, forums and pages that make hair-raising proclamations on the subject, very few of which have any factual basis in biology or physiology. As usual, let's start with a few actual examples:

  • "if you see a bit of pyramiding, its not the end of the world. It is purely cosmetic and your tortoise is not going to be less healthy because of it"

  • "Pyramiding doesn't have ANYTHING to do with feeding".

  • "If you see signs of pyramiding your tortoise needs a closed chamber now."

  • "Pyramiding does not happen in the wild because juveniles spend most of their time in humid hides where humidity is 80% or higher and temperatures rarely go below 30 Celsius"

  • "In order to keep the development of PGS (pyramiding growth syndrome) to a minimum, areas with a relative humidity of nearly 100% for hiding should be provided to the tortoises at all times"

Let's (as usual) address these specific points:

  • It is not 'purely cosmetic' and in captive animals almost invariably indicates that there is an underlying problerm with bone density and bone strength. The sole exceptions to this are wild tortoises, as we discuss here, where a conical scute growth formation is normal, for example, 'Tent' tortoises and certain other species where such a growth pattern is normal and typical in wild examples.

  • Yes - most cases of pyramiding do indeed have a lot to do with feeding as if the feeding regime being used results in metabolic bone disease or other bone growth deficiencies this in turn affects the strength of the bone, making it far more likely to deform under extended stresses.

  • Tortoises do not live in 'closed chambers'. If you are having to resort to such extreme methods there is something seriously wrong elsewhere.

  • Arid and semi-arid species do not have regular access to humid hides with 80% relative humidity. This is entirely false. So is the claim that temperatures rarely go below 30 Celsius. This is no more than an internet myth and is easily disproven.

  • If wild tortoises grow perfectly with smooth shells and excellent bone density without access to hides with 100% (or 80%) humidity, why would anyone assume that they need this in captivity?

This is a complex condition which involves both diet AND environment. We have written elsewhere on the precise mechanisms involved. However, to really simplify this you could think of it as a physical 'battle of strength' between the bones of the carapace and the layer of keratin which surrounds it. If the bones are weak and soft due to combinations of osteomalacia and ostodystrophy (i.e., various forms of Metabolic Bone Disease, most of which are caused by dietary deficiencies or excesses) then the continually applied physical stresses of the keratin (which is a very strong material indeed) will deform it easily. If, on the other hand, the bones are strong and dense, they resist these physical forces much more readily. Humidity plays a role because, as we know, keratin is incredibly hygroscopic. It is stiff when dry, but soft when wet and warm (as proved by taking a hot bath). So, if we over-dry it (under intense heat lamps) for example, we increase these stresses. The growing keratin effectively 'pulls' the underlying bones upwards due to the pattern of cell proliferation, or 'growth rings' that are a unique feature of tortoise anatomy. Incidentally, aquatic turtles have a different method of keratin cell proliferation than terrestrial tortoises, so this so-called 'pyramiding' issue is much less evident. They also shed whole scutes, which additionally helps to prevent very thick layers accumulating. Very thick keratin exerts incredibly powerful physical 'pulling power' on the underlying bones, so very often the worst cases of 'pyramiding' feature both weakened, defective bone tissue and unnaturally thickened keratin.

A further effect is exterted by both the internal, powerful muscles of the limbs inside the carapace, and also pressures from inside the shell resulting from lung expansion and contraction. These too can, over time, result in very specific manifestations of shell deformity. The weaker the bones are, the more obvious these effects become. See the very first picture headlining this article for an example.

It is worth noting, as mentioned, that there are some tortoises, from certain localities, where a similar raised scute format is normal for them, of course, e.g. the 'Tent tortoises' (genus Psammobates), of the arid regions of South Africa, and also some Leopard tortoises (Stigmochelys pardalis) from certain areas.

Two examples of 'Tent' tortoises (Psammobates) from arid regions of Southern Africa. Some degree of 'pyramiding' is quite normal for these species and does not indicate any underlying health issue.

What is going on here? Well, the exact same mechanisms are involved but in these cases there is no underlying pathology of the carapace. This is easily demonstrated if you examine road casualties, etc. Their bones are almost invariably of excellent strength and density (compared to captive tortoises with 'pathological pyramiding' where the bones are porous, fibrous and weak). Keratin is, however, an incredibly powerful material, and as we know, the drier it is the harder and stiffer it becomes. It is no coincidence, therefore, that the most extreme forms of natural (non-pathological) 'pyramiding' as seen in the Tent tortoises, some 'Star' tortoises and some Leopard tortoises almost precisely correlates with the reative aridity of the habitats that they are found in. Additionally, the keratin scutes in such tortoises tend to be rather thick (more than twice as thick in some cases) as other species (very probably as a mechanism to provide additional protection from subcutaneous fluid losses in extremely arid habitats) , thus amplifying the physical effects upon the bone beneath. The keratin scutes here are also often subject to very low levels of humidity, and even rarer episodes of rainfall, e,g., in the Karoo areas of Southern Africa. The extreme strength and 'pulling power' of these thicker keratin scutes in these very specific habitat conditions is, over time, capable of deforming even healthy, strong bone.

To demonstrate this, let's take a close look at the carapace bone condition of a wild-grown Stigmochelys pardalis (Leopard tortoise). The bone density here is excellent. There are no lesions. There is no abnormal fibrous tissue. As with Tent tortoises, however, in this particular example there is distinct 'pyramiding' of the vertebral series. Not all Leopard tortoises are like this. Some are very flat and smooth. This appears to correlate broadly with local environmental conditions. The more arid the area, the more frequently this appears to be observed. This is an interesting subject for further investigation and study in the field.

In the image below we can see a close-up section of the carapace bone confirming the excellent density and normal thickness of the carapace plates.

Looking specifically at the spinal-veterbral area, we can again confirm normal healthy bone tissue, even though it has 'followed' the physical forces exerted by the overlying keratin scutes. This image also confirms that the sutures between the bony plates are entirely normal and that the costal bones are also of excellent thickness and density, free of lesions or fibrous abnormalities.

A common (but entirely false) belief spread on many 'tortoise keeper' social media and internet groups is that "because we find 'pyramiding' in some wild species, this means that it is not a problem if our captive tortoises develop it". This is - we stress again - to completely misunderstand what is happening here. So-called 'pyramiding' is not a specific condition, but a syndrome with various causes. To concentrate upon the visible effect while ignoring the underlying causes is quite literally, an often fatal error. It would be better if perhaps we classified this effect into two separate groups. First, 'pathological pyramiding' which occurs as a result of incorrect diet and environments in captive animals, and 'environmental pyramiding' that is seen in certain specific species even when maintained under completely natural conditions. The two should not be conflated and confused. In the former case there are invariably serious underlying dietary and osteological problems present. In the latter case the diet may be entirely 'correct' and healhy, and there are NO BONE ABNORMALITIES PRESENT.

By contrast this is a typical example of 'pathological pyramiding' in a captive-raised Leopard tortoise on an inappropriate diet.

It must be stressed yet again, that 100% of all cases of carapace deformities (many hundreds) that we have studied over the past 40 years in captive tortoises have involved pathological bone disorders due to dietary deficiencies (calcium, D3) or excesses (protein levels, too-high digestibility, carbohydrates and phosphorus). We have not encountered a single case where this was not so.

It is, therefore, vitally important to differentiate between certain species from particular habitats where a raised scute format is normal for that species in that habitat, without underlying pathologies, and those species where the normal (wild) carapace development is smooth, but that in captivity manifest raised scutes in combination with various forms of metabolic bone disease. It is a completely false argument to suggest, for example, that just because the tent tortoises (Psammobates) demonstrate a raised ('pyramid') scute format that this is normal or should be accepted in say, Testudo graeca or Centrochelys sulcata. It isn't, and it should not be.


It is not hard to avoid this:

Avoid any diet (or feeding quantity) that results in highly accelerated rates of growth. High growth rates are typically associated with a greatly increased incidence of MBD (metabolic bone disease) in all of its possible forms and combinations. One reason for this, in very simple terms, is that it is difficult to ensure good bone density if the growth rate is too fast. Supplying the essential minerals and other components required in balanced amounts becomes harder and harder when 'runaway' growth occurs. Juveniles are highly sensitive to even slight deficiencies or imbalances, and so they are particularly vulnerable to develop bone density problems very rapidly indeed. Adults already have an established skeleton, and this acts as a 'buffer' that can see them 'ride' out temporary deficiencies. Hatchlings and young juveniles do not. Poor bone density equates directly to weak bone, and this is exceptionally vulnerable to both internal (muscular) and external (keratin) stressors that effectively 'warp' it - this is what we are seeing in such cases.

To summarise:

  • Never underestimate or minimise how serious this is. Many of the worst effects are only visible by x-ray or via post-mortem, internally.

  • This is almost 100% preventable with the correct diet (which varies by species) and by giving adequate attention to environmental factors such as proper provision of UV-B and by avoiding environmental 'aggravating factors' such excessively 'drying' artificial heat sources and unusuitable forms of accommodation.

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(C) A. C. Highfield/Tortoise Trust 2024

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